A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
Peptides generated from AMYLOID BETA-PEPTIDES PRECURSOR. An amyloid fibrillar form of these peptides is the major component of amyloid plaques found in individuals with Alzheimer's disease and in aged individuals with trisomy 21 (DOWN SYNDROME). The peptide is found predominantly in the nervous system, but there have been reports of its presence in non-neural tissue.
Microtubule-associated proteins that are mainly expressed in neurons. Tau proteins constitute several isoforms and play an important role in the assembly of tubulin monomers into microtubules and in maintaining the cytoskeleton and axonal transport. Aggregation of specific sets of tau proteins in filamentous inclusions is the common feature of intraneuronal and glial fibrillar lesions (NEUROFIBRILLARY TANGLES; NEUROPIL THREADS) in numerous neurodegenerative disorders (ALZHEIMER DISEASE; TAUOPATHIES).
A single-pass type I membrane protein. It is cleaved by AMYLOID PRECURSOR PROTEIN SECRETASES to produce peptides of varying amino acid lengths. A 39-42 amino acid peptide, AMYLOID BETA-PEPTIDES is a principal component of the extracellular amyloid in SENILE PLAQUES.
Abnormal structures located in various parts of the brain and composed of dense arrays of paired helical filaments (neurofilaments and microtubules). These double helical stacks of transverse subunits are twisted into left-handed ribbon-like filaments that likely incorporate the following proteins: (1) the intermediate filaments: medium- and high-molecular-weight neurofilaments; (2) the microtubule-associated proteins map-2 and tau; (3) actin; and (4) UBIQUITINS. As one of the hallmarks of ALZHEIMER DISEASE, the neurofibrillary tangles eventually occupy the whole of the cytoplasm in certain classes of cell in the neocortex, hippocampus, brain stem, and diencephalon. The number of these tangles, as seen in post mortem histology, correlates with the degree of dementia during life. Some studies suggest that tangle antigens leak into the systemic circulation both in the course of normal aging and in cases of Alzheimer disease.
Accumulations of extracellularly deposited AMYLOID FIBRILS within tissues.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
A major and the second most common isoform of apolipoprotein E. In humans, Apo E4 differs from APOLIPOPROTEIN E3 at only one residue 112 (cysteine is replaced by arginine), and exhibits a lower resistance to denaturation and greater propensity to form folded intermediates. Apo E4 is a risk factor for ALZHEIMER DISEASE and CARDIOVASCULAR DISEASES.
Endopeptidases that are specific for AMYLOID PROTEIN PRECURSOR. Three secretase subtypes referred to as alpha, beta, and gamma have been identified based upon the region of amyloid protein precursor they cleave.
Disturbances in mental processes related to learning, thinking, reasoning, and judgment.
An acquired organic mental disorder with loss of intellectual abilities of sufficient severity to interfere with social or occupational functioning. The dysfunction is multifaceted and involves memory, behavior, personality, judgment, attention, spatial relations, language, abstract thought, and other executive functions. The intellectual decline is usually progressive, and initially spares the level of consciousness.
Integral membrane protein of Golgi and endoplasmic reticulum. Its homodimer is an essential component of the gamma-secretase complex that catalyzes the cleavage of membrane proteins such as NOTCH RECEPTORS and AMYLOID BETA-PEPTIDES precursors. PSEN1 mutations cause early-onset ALZHEIMER DISEASE type 3 that may occur as early as 30 years of age in humans.
A fibrous protein complex that consists of proteins folded into a specific cross beta-pleated sheet structure. This fibrillar structure has been found as an alternative folding pattern for a variety of functional proteins. Deposits of amyloid in the form of AMYLOID PLAQUES are associated with a variety of degenerative diseases. The amyloid structure has also been found in a number of functional proteins that are unrelated to disease.
Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.
An imprecise term referring to dementia associated with CEREBROVASCULAR DISORDERS, including CEREBRAL INFARCTION (single or multiple), and conditions associated with chronic BRAIN ISCHEMIA. Diffuse, cortical, and subcortical subtypes have been described. (From Gerontol Geriatr 1998 Feb;31(1):36-44)
Tests designed to assess neurological function associated with certain behaviors. They are used in diagnosing brain dysfunction or damage and central nervous system disorders or injury.
The delicate interlacing threads, formed by aggregations of neurofilaments and neurotubules, coursing through the CYTOPLASM of the body of a NEURON and extending from one DENDRITE into another or into the AXON.
A prodromal phase of cognitive decline that may precede the emergence of ALZHEIMER DISEASE and other dementias. It may include impairment of cognition, such as impairments in language, visuospatial awareness, ATTENTION and MEMORY.
A class of protein components which can be found in several lipoproteins including HIGH-DENSITY LIPOPROTEINS; VERY-LOW-DENSITY LIPOPROTEINS; and CHYLOMICRONS. Synthesized in most organs, Apo E is important in the global transport of lipids and cholesterol throughout the body. Apo E is also a ligand for LDL receptors (RECEPTORS, LDL) that mediates the binding, internalization, and catabolism of lipoprotein particles in cells. There are several allelic isoforms (such as E2, E3, and E4). Deficiency or defects in Apo E are causes of HYPERLIPOPROTEINEMIA TYPE III.
Integral membrane protein of Golgi and endoplasmic reticulum. Its homodimer is an essential component of the gamma-secretase complex that catalyzes the cleavage of membrane proteins such as NOTCH RECEPTORS and AMYLOID BETA-PEPTIDES precursors. PSEN2 mutations cause ALZHEIMER DISEASE type 4.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
Standardized clinical interview used to assess current psychopathology by scaling patient responses to the questions.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
Intellectual or mental process whereby an organism obtains knowledge.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
A neurodegenerative disease characterized by dementia, mild parkinsonism, and fluctuations in attention and alertness. The neuropsychiatric manifestations tend to precede the onset of bradykinesia, MUSCLE RIGIDITY, and other extrapyramidal signs. DELUSIONS and visual HALLUCINATIONS are relatively frequent in this condition. Histologic examination reveals LEWY BODIES in the CEREBRAL CORTEX and BRAIN STEM. SENILE PLAQUES and other pathologic features characteristic of ALZHEIMER DISEASE may also be present. (From Neurology 1997;48:376-380; Neurology 1996;47:1113-1124)
AMANTADINE derivative that has some dopaminergic effects. It has been proposed as an antiparkinson agent.
The age, developmental stage, or period of life at which a disease or the initial symptoms or manifestations of a disease appear in an individual.
Integral membrane proteins and essential components of the gamma-secretase complex that catalyzes the cleavage of membrane proteins such as NOTCH RECEPTORS and AMYLOID BETA-PEPTIDES precursors. Mutations of presenilins lead to presenile ALZHEIMER DISEASE with onset before age 65 years.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
A sub-subclass of endopeptidases that depend on an ASPARTIC ACID residue for their activity.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Drugs that inhibit cholinesterases. The neurotransmitter ACETYLCHOLINE is rapidly hydrolyzed, and thereby inactivated, by cholinesterases. When cholinesterases are inhibited, the action of endogenously released acetylcholine at cholinergic synapses is potentiated. Cholinesterase inhibitors are widely used clinically for their potentiation of cholinergic inputs to the gastrointestinal tract and urinary bladder, the eye, and skeletal muscles; they are also used for their effects on the heart and the central nervous system.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
Component of the NATIONAL INSTITUTES OF HEALTH. Through basic and clinical biomedical research and training, it conducts and supports research into the nature of the aging process and diseases associated with the later stages of life. The Institute was established in 1974.
Tissue in the BASAL FOREBRAIN inferior to the anterior perforated substance, and anterior to the GLOBUS PALLIDUS and ansa lenticularis. It contains the BASAL NUCLEUS OF MEYNERT.
Disturbances in registering an impression, in the retention of an acquired impression, or in the recall of an impression. Memory impairments are associated with DEMENTIA; CRANIOCEREBRAL TRAUMA; ENCEPHALITIS; ALCOHOLISM (see also ALCOHOL AMNESTIC DISORDER); SCHIZOPHRENIA; and other conditions.
The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.
A heterogeneous group of sporadic or familial disorders characterized by AMYLOID deposits in the walls of small and medium sized blood vessels of CEREBRAL CORTEX and MENINGES. Clinical features include multiple, small lobar CEREBRAL HEMORRHAGE; cerebral ischemia (BRAIN ISCHEMIA); and CEREBRAL INFARCTION. Cerebral amyloid angiopathy is unrelated to generalized AMYLOIDOSIS. Amyloidogenic peptides in this condition are nearly always the same ones found in ALZHEIMER DISEASE. (from Kumar: Robbins and Cotran: Pathologic Basis of Disease, 7th ed., 2005)
Studies in which variables relating to an individual or group of individuals are assessed over a period of time.
Proteins that form the core of amyloid fibrils. For example, the core of amyloid A is formed from amyloid A protein, also known as serum amyloid A protein or SAA protein.
Postmortem examination of the body.
Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.
An imaging technique using compounds labelled with short-lived positron-emitting radionuclides (such as carbon-11, nitrogen-13, oxygen-15 and fluorine-18) to measure cell metabolism. It has been useful in study of soft tissues such as CANCER; CARDIOVASCULAR SYSTEM; and brain. SINGLE-PHOTON EMISSION-COMPUTED TOMOGRAPHY is closely related to positron emission tomography, but uses isotopes with longer half-lives and resolution is lower.
The worsening of a disease over time. This concept is most often used for chronic and incurable diseases where the stage of the disease is an important determinant of therapy and prognosis.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
Extracellular protease inhibitors that are secreted from FIBROBLASTS. They form a covalent complex with SERINE PROTEASES and can mediate their cellular internalization and degradation.
Clinical or physiological indicators that precede the onset of disease.
Phenyl esters of carbamic acid or of N-substituted carbamic acids. Structures are similar to PHENYLUREA COMPOUNDS with a carbamate in place of the urea.
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
Neurodegenerative disorders involving deposition of abnormal tau protein isoforms (TAU PROTEINS) in neurons and glial cells in the brain. Pathological aggregations of tau proteins are associated with mutation of the tau gene on chromosome 17 in patients with ALZHEIMER DISEASE; DEMENTIA; PARKINSONIAN DISORDERS; progressive supranuclear palsy (SUPRANUCLEAR PALSY, PROGRESSIVE); and corticobasal degeneration.
Hereditary and sporadic conditions which are characterized by progressive nervous system dysfunction. These disorders are often associated with atrophy of the affected central or peripheral nervous system structures.
Aryl CYCLOPENTANES that are a reduced (protonated) form of INDENES.
Drugs used to specifically facilitate learning or memory, particularly to prevent the cognitive deficits associated with dementias. These drugs act by a variety of mechanisms. While no potent nootropic drugs have yet been accepted for general use, several are being actively investigated.
A chromosome disorder associated either with an extra chromosome 21 or an effective trisomy for chromosome 21. Clinical manifestations include hypotonia, short stature, brachycephaly, upslanting palpebral fissures, epicanthus, Brushfield spots on the iris, protruding tongue, small ears, short, broad hands, fifth finger clinodactyly, Simian crease, and moderate to severe INTELLECTUAL DISABILITY. Cardiac and gastrointestinal malformations, a marked increase in the incidence of LEUKEMIA, and the early onset of ALZHEIMER DISEASE are also associated with this condition. Pathologic features include the development of NEUROFIBRILLARY TANGLES in neurons and the deposition of AMYLOID BETA-PROTEIN, similar to the pathology of ALZHEIMER DISEASE. (Menkes, Textbook of Child Neurology, 5th ed, p213)
A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.
Intracytoplasmic, eosinophilic, round to elongated inclusions found in vacuoles of injured or fragmented neurons. The presence of Lewy bodies is the histological marker of the degenerative changes in LEWY BODY DISEASE and PARKINSON DISEASE but they may be seen in other neurological conditions. They are typically found in the substantia nigra and locus coeruleus but they are also seen in the basal forebrain, hypothalamic nuclei, and neocortex.
A potentially neurotoxic 8-hydroxyquinoline derivative long used as a topical anti-infective, intestinal antiamebic, and vaginal trichomonacide. The oral preparation has been shown to cause subacute myelo-optic neuropathy and has been banned worldwide.
The most common clinical form of FRONTOTEMPORAL LOBAR DEGENERATION, this dementia presents with personality and behavioral changes often associated with disinhibition, apathy, and lack of insight.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
Pathologic partial or complete loss of the ability to recall past experiences (AMNESIA, RETROGRADE) or to form new memories (AMNESIA, ANTEROGRADE). This condition may be of organic or psychologic origin. Organic forms of amnesia are usually associated with dysfunction of the DIENCEPHALON or HIPPOCAMPUS. (From Adams et al., Principles of Neurology, 6th ed, pp426-7)
The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.
Lower lateral part of the cerebral hemisphere responsible for auditory, olfactory, and semantic processing. It is located inferior to the lateral fissure and anterior to the OCCIPITAL LOBE.
A feeling of restlessness associated with increased motor activity. This may occur as a manifestation of nervous system drug toxicity or other conditions.
Abnormal structures located chiefly in distal dendrites and, along with NEUROFIBRILLARY TANGLES and SENILE PLAQUES, constitute the three morphological hallmarks of ALZHEIMER DISEASE. Neuropil threads are made up of straight and paired helical filaments which consist of abnormally phosphorylated microtubule-associated tau proteins. It has been suggested that the threads have a major role in the cognitive impairment seen in Alzheimer disease.
Studies which start with the identification of persons with a disease of interest and a control (comparison, referent) group without the disease. The relationship of an attribute to the disease is examined by comparing diseased and non-diseased persons with regard to the frequency or levels of the attribute in each group.
Studies in which subsets of a defined population are identified. These groups may or may not be exposed to factors hypothesized to influence the probability of the occurrence of a particular disease or other outcome. Cohorts are defined populations which, as a whole, are followed in an attempt to determine distinguishing subgroup characteristics.
An enzyme the catalyzes the degradation of insulin, glucagon and other polypeptides. It is inhibited by bacitracin, chelating agents EDTA and 1,10-phenanthroline, and by thiol-blocking reagents such as N-ethylmaleimide, but not phosphoramidon. (Eur J Biochem 1994;223:1-5) EC
A 34-kDa glycosylated protein. A major and most common isoform of apolipoprotein E. Therefore, it is also known as apolipoprotein E (ApoE). In human, Apo E3 is a 299-amino acid protein with a cysteine at the 112 and an arginine at the 158 position. It is involved with the transport of TRIGLYCERIDES; PHOSPHOLIPIDS; CHOLESTEROL; and CHOLESTERYL ESTERS in and out of the cells.
A cholinesterase inhibitor that crosses the blood-brain barrier. Tacrine has been used to counter the effects of muscle relaxants, as a respiratory stimulant, and in the treatment of Alzheimer's disease and other central nervous system disorders.
Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory.
A specific pair of GROUP G CHROMOSOMES of the human chromosome classification.
A subclass of clathrin assembly proteins that occur as monomers.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
The range or frequency distribution of a measurement in a population (of organisms, organs or things) that has not been selected for the presence of disease or abnormality.
A progressive, degenerative neurologic disease characterized by a TREMOR that is maximal at rest, retropulsion (i.e. a tendency to fall backwards), rigidity, stooped posture, slowness of voluntary movements, and a masklike facial expression. Pathologic features include loss of melanin containing neurons in the substantia nigra and other pigmented nuclei of the brainstem. LEWY BODIES are present in the substantia nigra and locus coeruleus but may also be found in a related condition (LEWY BODY DISEASE, DIFFUSE) characterized by dementia in combination with varying degrees of parkinsonism. (Adams et al., Principles of Neurology, 6th ed, p1059, pp1067-75)
Any detectable and heritable change in the genetic material that causes a change in the GENOTYPE and which is transmitted to daughter cells and to succeeding generations.
One of three major isoforms of apolipoprotein E. In humans, Apo E2 differs from APOLIPOPROTEIN E3 at one residue 158 where arginine is replaced by cysteine (R158--C). In contrast to Apo E3, Apo E2 displays extremely low binding affinity for LDL receptors (RECEPTORS, LDL) which mediate the internalization and catabolism of lipoprotein particles in liver cells. ApoE2 allelic homozygosity is associated with HYPERLIPOPROTEINEMIA TYPE III.
A neurobehavioral syndrome associated with bilateral medial temporal lobe dysfunction. Clinical manifestations include oral exploratory behavior; tactile exploratory behavior; hypersexuality; BULIMIA; MEMORY DISORDERS; placidity; and an inability to recognize objects or faces. This disorder may result from a variety of conditions, including CRANIOCEREBRAL TRAUMA; infections; ALZHEIMER DISEASE; PICK DISEASE OF THE BRAIN; and CEREBROVASCULAR DISORDERS.
A benzazepine derived from norbelladine. It is found in GALANTHUS and other AMARYLLIDACEAE. It is a cholinesterase inhibitor that has been used to reverse the muscular effects of GALLAMINE TRIETHIODIDE and TUBOCURARINE and has been studied as a treatment for ALZHEIMER DISEASE and other central nervous system disorders.
An aspect of personal behavior or lifestyle, environmental exposure, or inborn or inherited characteristic, which, on the basis of epidemiologic evidence, is known to be associated with a health-related condition considered important to prevent.
Heterogeneous group of neurodegenerative disorders characterized by frontal and temporal lobe atrophy associated with neuronal loss, gliosis, and dementia. Patients exhibit progressive changes in social, behavioral, and/or language function. Multiple subtypes or forms are recognized based on presence or absence of TAU PROTEIN inclusions. FTLD includes three clinical syndromes: FRONTOTEMPORAL DEMENTIA, semantic dementia, and PRIMARY PROGRESSIVE NONFLUENT APHASIA.
Compounds with a benzene ring fused to a thiazole ring.
Detection of a MUTATION; GENOTYPE; KARYOTYPE; or specific ALLELES associated with genetic traits, heritable diseases, or predisposition to a disease, or that may lead to the disease in descendants. It includes prenatal genetic testing.
A neuronal calcium sensor protein that is expressed as several isoforms and can interact with ACTIN; TUBULIN; and CLATHRIN.
A group of sporadic, familial and/or inherited, degenerative, and infectious disease processes, linked by the common theme of abnormal protein folding and deposition of AMYLOID. As the amyloid deposits enlarge they displace normal tissue structures, causing disruption of function. Various signs and symptoms depend on the location and size of the deposits.
A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).
A subsection of the hippocampus, described by Lorente de No, that is located between the HIPPOCAMPUS CA1 FIELD and the HIPPOCAMPUS CA3 FIELD.
A class of nerve fibers as defined by their structure, specifically the nerve sheath arrangement. The AXONS of the myelinated nerve fibers are completely encased in a MYELIN SHEATH. They are fibers of relatively large and varied diameters. Their NEURAL CONDUCTION rates are faster than those of the unmyelinated nerve fibers (NERVE FIBERS, UNMYELINATED). Myelinated nerve fibers are present in somatic and autonomic nerves.
Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.
A glycogen synthase kinase that was originally described as a key enzyme involved in glycogen metabolism. It regulates a diverse array of functions such as CELL DIVISION, microtubule function and APOPTOSIS.
Persons who provide care to those who need supervision or assistance in illness or disability. They may provide the care in the home, in a hospital, or in an institution. Although caregivers include trained medical, nursing, and other health personnel, the concept also refers to parents, spouses, or other family members, friends, members of the clergy, teachers, social workers, fellow patients.
Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.
A serine-threonine kinase that plays important roles in CELL DIFFERENTIATION; CELL MIGRATION; and CELL DEATH of NERVE CELLS. It is closely related to other CYCLIN-DEPENDENT KINASES but does not seem to participate in CELL CYCLE regulation.
Physiological changes that occur in bodies after death.
Theoretical representations that simulate the behavior or activity of biological processes or diseases. For disease models in living animals, DISEASE MODELS, ANIMAL is available. Biological models include the use of mathematical equations, computers, and other electronic equipment.
Cerebral cortex region on the medial aspect of the PARAHIPPOCAMPAL GYRUS, immediately caudal to the OLFACTORY CORTEX of the uncus. The entorhinal cortex is the origin of the major neural fiber system afferent to the HIPPOCAMPAL FORMATION, the so-called PERFORANT PATHWAY.
A republic in the Greater Antilles in the West Indies. Its capital is Santo Domingo. With Haiti, it forms the island of Hispaniola - the Dominican Republic occupying the eastern two thirds, and Haiti, the western third. It was created in 1844 after a revolt against the rule of President Boyer over the entire island of Hispaniola, itself visited by Columbus in 1492 and settled the next year. Except for a brief period of annexation to Spain (1861-65), it has been independent, though closely associated with the United States. Its name comes from the Spanish Santo Domingo, Holy Sunday, with reference to its discovery on a Sunday. (From Webster's New Geographical Dictionary, 1988, p338, 506 & Room, Brewer's Dictionary of Names, 1992, p151)
The part of the cerebral hemisphere anterior to the central sulcus, and anterior and superior to the lateral sulcus.
A highly conserved heterodimeric glycoprotein that is differentially expressed during many severe physiological disturbance states such as CANCER; APOPTOSIS; and various NEUROLOGICAL DISORDERS. Clusterin is ubiquitously expressed and appears to function as a secreted MOLECULAR CHAPERONE.
Standardized procedures utilizing rating scales or interview schedules carried out by health personnel for evaluating the degree of mental illness.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
Age as a constituent element or influence contributing to the production of a result. It may be applicable to the cause or the effect of a circumstance. It is used with human or animal concepts but should be differentiated from AGING, a physiological process, and TIME FACTORS which refers only to the passage of time.
A technique of inputting two-dimensional images into a computer and then enhancing or analyzing the imagery into a form that is more useful to the human observer.
The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
The order of amino acids as they occur in a polypeptide chain. This is referred to as the primary structure of proteins. It is of fundamental importance in determining PROTEIN CONFORMATION.
A CELL LINE derived from a PHEOCHROMOCYTOMA of the rat ADRENAL MEDULLA. PC12 cells stop dividing and undergo terminal differentiation when treated with NERVE GROWTH FACTOR, making the line a useful model system for NERVE CELL differentiation.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.
Learning the correct route through a maze to obtain reinforcement. It is used for human or animal populations. (Thesaurus of Psychological Index Terms, 6th ed)
The area that lies between continental North and South America and comprises the Caribbean Sea, the West Indies, and the adjacent mainland regions of southern Mexico, Central America, Colombia, and Venezuela.
The process in which substances, either endogenous or exogenous, bind to proteins, peptides, enzymes, protein precursors, or allied compounds. Specific protein-binding measures are often used as assays in diagnostic assessments.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98.
Normal cellular isoform of prion proteins (PRIONS) encoded by a chromosomal gene and found in normal and scrapie-infected brain tissue, and other normal tissue. PrPC are protease-sensitive proteins whose function is unknown. Posttranslational modification of PrPC into PrPSC leads to infectivity.
A short pro-domain caspase that plays an effector role in APOPTOSIS. It is activated by INITIATOR CASPASES such as CASPASE 7; CASPASE 8; and CASPASE 10. Isoforms of this protein exist due to multiple alternative splicing of its MESSENGER RNA.
High molecular weight proteins found in the MICROTUBULES of the cytoskeletal system. Under certain conditions they are required for TUBULIN assembly into the microtubules and stabilize the assembled microtubules.
Vaccines or candidate vaccines used to prevent or treat ALZHEIMER DISEASE.
The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.
Proteins which are found in membranes including cellular and intracellular membranes. They consist of two types, peripheral and integral proteins. They include most membrane-associated enzymes, antigenic proteins, transport proteins, and drug, hormone, and lectin receptors.
The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion.
The statistical reproducibility of measurements (often in a clinical context), including the testing of instrumentation or techniques to obtain reproducible results. The concept includes reproducibility of physiological measurements, which may be used to develop rules to assess probability or prognosis, or response to a stimulus; reproducibility of occurrence of a condition; and reproducibility of experimental results.
Type III intermediate filament proteins that assemble into neurofilaments, the major cytoskeletal element in nerve axons and dendrites. They consist of three distinct polypeptides, the neurofilament triplet. Types I, II, and IV intermediate filament proteins form other cytoskeletal elements such as keratins and lamins. It appears that the metabolism of neurofilaments is disturbed in Alzheimer's disease, as indicated by the presence of neurofilament epitopes in the neurofibrillary tangles, as well as by the severe reduction of the expression of the gene for the light neurofilament subunit of the neurofilament triplet in brains of Alzheimer's patients. (Can J Neurol Sci 1990 Aug;17(3):302)
A progressive form of dementia characterized by the global loss of language abilities and initial preservation of other cognitive functions. Fluent and nonfluent subtypes have been described. Eventually a pattern of global cognitive dysfunction, similar to ALZHEIMER DISEASE, emerges. Pathologically, there are no Alzheimer or PICK DISEASE like changes, however, spongiform changes of cortical layers II and III are present in the TEMPORAL LOBE and FRONTAL LOBE. (From Brain 1998 Jan;121(Pt 1):115-26)
Small proteinaceous infectious particles which resist inactivation by procedures that modify NUCLEIC ACIDS and contain an abnormal isoform of a cellular protein which is a major and necessary component. The abnormal (scrapie) isoform is PrPSc (PRPSC PROTEINS) and the cellular isoform PrPC (PRPC PROTEINS). The primary amino acid sequence of the two isoforms is identical. Human diseases caused by prions include CREUTZFELDT-JAKOB SYNDROME; GERSTMANN-STRAUSSLER SYNDROME; and INSOMNIA, FATAL FAMILIAL.
A genus of the family Lemuridae consisting of five species: L. catta (ring-tailed lemur), L. fulvus, L. macaco (acoumba or black lemur), L. mongoz (mongoose lemur), and L. variegatus (white lemur). Most members of this genus occur in forested areas on Madagascar and the Comoro Islands.
The compound is given by intravenous injection to do POSITRON-EMISSION TOMOGRAPHY for the assessment of cerebral and myocardial glucose metabolism in various physiological or pathological states including stroke and myocardial ischemia. It is also employed for the detection of malignant tumors including those of the brain, liver, and thyroid gland. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1162)
The health status of the family as a unit including the impact of the health of one member of the family on the family as a unit and on individual family members; also, the impact of family organization or disorganization on the health status of its members.
The assembly of the QUATERNARY PROTEIN STRUCTURE of multimeric proteins (MULTIPROTEIN COMPLEXES) from their composite PROTEIN SUBUNITS.
Four CSF-filled (see CEREBROSPINAL FLUID) cavities within the cerebral hemispheres (LATERAL VENTRICLES), in the midline (THIRD VENTRICLE) and within the PONS and MEDULLA OBLONGATA (FOURTH VENTRICLE).
In screening and diagnostic tests, the probability that a person with a positive test is a true positive (i.e., has the disease), is referred to as the predictive value of a positive test; whereas, the predictive value of a negative test is the probability that the person with a negative test does not have the disease. Predictive value is related to the sensitivity and specificity of the test.
The ability of a substance to be dissolved, i.e. to form a solution with another substance. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
The level of protein structure in which combinations of secondary protein structures (alpha helices, beta sheets, loop regions, and motifs) pack together to form folded shapes called domains. Disulfide bridges between cysteines in two different parts of the polypeptide chain along with other interactions between the chains play a role in the formation and stabilization of tertiary structure. Small proteins usually consist of only one domain but larger proteins may contain a number of domains connected by segments of polypeptide chain which lack regular secondary structure.
Cleavage of proteins into smaller peptides or amino acids either by PROTEASES or non-enzymatically (e.g., Hydrolysis). It does not include Protein Processing, Post-Translational.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Elements of limited time intervals, contributing to particular results or situations.
A convolution on the inferior surface of each cerebral hemisphere, lying between the hippocampal and collateral sulci.
An acid dye used in testing for hydrochloric acid in gastric contents. It is also used histologically to test for AMYLOIDOSIS.
An analysis comparing the allele frequencies of all available (or a whole GENOME representative set of) polymorphic markers in unrelated patients with a specific symptom or disease condition, and those of healthy controls to identify markers associated with a specific disease or condition.
An immunoassay utilizing an antibody labeled with an enzyme marker such as horseradish peroxidase. While either the enzyme or the antibody is bound to an immunosorbent substrate, they both retain their biologic activity; the change in enzyme activity as a result of the enzyme-antibody-antigen reaction is proportional to the concentration of the antigen and can be measured spectrophotometrically or with the naked eye. Many variations of the method have been developed.
A subclass of PEPTIDE HYDROLASES that catalyze the internal cleavage of PEPTIDES or PROTEINS.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Studies in which individuals or populations are followed to assess the outcome of exposures, procedures, or effects of a characteristic, e.g., occurrence of disease.
Slow or diminished movement of body musculature. It may be associated with BASAL GANGLIA DISEASES; MENTAL DISORDERS; prolonged inactivity due to illness; and other conditions.
Binary classification measures to assess test results. Sensitivity or recall rate is the proportion of true positives. Specificity is the probability of correctly determining the absence of a condition. (From Last, Dictionary of Epidemiology, 2d ed)
Members of the class of compounds composed of AMINO ACIDS joined together by peptide bonds between adjacent amino acids into linear, branched or cyclical structures. OLIGOPEPTIDES are composed of approximately 2-12 amino acids. Polypeptides are composed of approximately 13 or more amino acids. PROTEINS are linear polypeptides that are normally synthesized on RIBOSOMES.
Any of various enzymatically catalyzed post-translational modifications of PEPTIDES or PROTEINS in the cell of origin. These modifications include carboxylation; HYDROXYLATION; ACETYLATION; PHOSPHORYLATION; METHYLATION; GLYCOSYLATION; ubiquitination; oxidation; proteolysis; and crosslinking and result in changes in molecular weight and electrophoretic motility.
A synuclein that is a major component of LEWY BODIES that plays a role in neurodegeneration and neuroprotection.
A form of compensated hydrocephalus characterized clinically by a slowly progressive gait disorder (see GAIT DISORDERS, NEUROLOGIC), progressive intellectual decline, and URINARY INCONTINENCE. Spinal fluid pressure tends to be in the high normal range. This condition may result from processes which interfere with the absorption of CSF including SUBARACHNOID HEMORRHAGE, chronic MENINGITIS, and other conditions. (From Adams et al., Principles of Neurology, 6th ed, pp631-3)
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
Established cell cultures that have the potential to propagate indefinitely.
Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.
Methods to determine in patients the nature of a disease or disorder at its early stage of progression. Generally, early diagnosis improves PROGNOSIS and TREATMENT OUTCOME.
Licensed physicians trained in OSTEOPATHIC MEDICINE. An osteopathic physician, also known as D.O. (Doctor of Osteopathy), is able to perform surgery and prescribe medications.
A familial disorder inherited as an autosomal dominant trait and characterized by the onset of progressive CHOREA and DEMENTIA in the fourth or fifth decade of life. Common initial manifestations include paranoia; poor impulse control; DEPRESSION; HALLUCINATIONS; and DELUSIONS. Eventually intellectual impairment; loss of fine motor control; ATHETOSIS; and diffuse chorea involving axial and limb musculature develops, leading to a vegetative state within 10-15 years of disease onset. The juvenile variant has a more fulminant course including SEIZURES; ATAXIA; dementia; and chorea. (From Adams et al., Principles of Neurology, 6th ed, pp1060-4)
The circulation of blood through the BLOOD VESSELS of the BRAIN.
An ethylene compound with two hydroxy groups (-OH) located on adjacent carbons. They are viscous and colorless liquids. Some are used as anesthetics or hypnotics. However, the class is best known for their use as a coolant or antifreeze.
Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.
Enzyme that is a major constituent of kidney brush-border membranes and is also present to a lesser degree in the brain and other tissues. It preferentially catalyzes cleavage at the amino group of hydrophobic residues of the B-chain of insulin as well as opioid peptides and other biologically active peptides. The enzyme is inhibited primarily by EDTA, phosphoramidon, and thiorphan and is reactivated by zinc. Neprilysin is identical to common acute lymphoblastic leukemia antigen (CALLA Antigen), an important marker in the diagnosis of human acute lymphocytic leukemia. There is no relationship with CALLA PLANT.
Uncrossed tracts of motor nerves from the brain to the anterior horns of the spinal cord, involved in reflexes, locomotion, complex movements, and postural control.
An individual having different alleles at one or more loci regarding a specific character.
Capacity that enables an individual to cope with and/or recover from the impact of a neural injury or a psychotic episode.
Active immunization where vaccine is administered for therapeutic or preventive purposes. This can include administration of immunopotentiating agents such as BCG vaccine and Corynebacterium parvum as well as biological response modifiers such as interferons, interleukins, and colony-stimulating factors in order to directly stimulate the immune system.
In tissue culture, hairlike projections of neurons stimulated by growth factors and other molecules. These projections may go on to form a branched tree of dendrites or a single axon or they may be reabsorbed at a later stage of development. "Neurite" may refer to any filamentous or pointed outgrowth of an embryonal or tissue-culture neural cell.
A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.
A scale comprising 18 symptom constructs chosen to represent relatively independent dimensions of manifest psychopathology. The initial intended use was to provide more efficient assessment of treatment response in clinical psychopharmacology research; however, the scale was readily adapted to other uses. (From Hersen, M. and Bellack, A.S., Dictionary of Behavioral Assessment Techniques, p. 87)
An enzyme that catalyzes the hydrolysis of ACETYLCHOLINE to CHOLINE and acetate. In the CNS, this enzyme plays a role in the function of peripheral neuromuscular junctions. EC
A cell line generated from human embryonic kidney cells that were transformed with human adenovirus type 5.
Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.

Alzheimer's disease: clues from flies and worms. (1/11292)

Presenilin mutations give rise to familial Alzheimer's disease and result in elevated production of amyloid beta peptide. Recent evidence that presenilins act in developmental signalling pathways may be the key to understanding how senile plaques, neurofibrillary tangles and apoptosis are all biochemically linked.  (+info)

Parametric mapping of cerebral blood flow deficits in Alzheimer's disease: a SPECT study using HMPAO and image standardization technique. (2/11292)

This study assessed the accuracy and reliability of Automated Image Registration (AIR) for standardization of brain SPECT images of patients with Alzheimer's disease (AD). Standardized cerebral blood flow (CBF) images of patients with AD and control subjects were then used for group comparison and covariance analyses. METHODS: Thirteen patients with AD at an early stage (age 69.8+/-7.1 y, Clinical Dementia Rating Score 0.5-1.0, Mini-Mental State Examination score 19-23) and 20 age-matched normal subjects (age 69.5+/-8.3 y) participated in this study. 99mTc-hexamethyl propylenamine oxime (HMPAO) brain SPECT and CT scans were acquired for each subject. SPECT images were transformed to a standard size and shape with the help of AIR. Accuracy of AIR for spatial normalization was evaluated by an index calculated on SPECT images. Anatomical variability of standardized target images was evaluated by measurements on corresponding CT scans, spatially normalized using transformations established by the SPECT images. Realigned brain SPECT images of patients and controls were used for group comparison with the help of statistical parameter mapping. Significant differences were displayed on the respective voxel to generate three-dimensional Z maps. CT scans of individual subjects were evaluated by a computer program for brain atrophy. Voxel-based covariance analysis was performed on standardized images with ages and atrophy indices as independent variables. RESULTS: Inaccuracy assessed by functional data was 2.3%. The maximum anatomical variability was 4.9 mm after standardization. Z maps showed significantly decreased regional CBF (rCBF) in the frontal, parietal and temporal regions in the patient group (P < 0.001). Covariance analysis revealed that the effects of aging on rCBF were more pronounced compared with atrophy, especially in intact cortical areas at an early stage of AD. Decrease in rCBF was partly due to senility and atrophy, however these two factors cannot explain all the deficits. CONCLUSION: AIR can transform SPECT images of AD patients with acceptable accuracy without any need for corresponding structural images. The frontal regions of the brain, in addition to parietal and temporal lobes, may show reduced CBF in patients with AD even at an early stage of dementia. The reduced rCBF in the cortical regions cannot be explained entirely by advanced atrophy and fast aging process.  (+info)

Proteolytic processing of the Alzheimer's disease amyloid precursor protein within its cytoplasmic domain by caspase-like proteases. (3/11292)

Alzheimer's disease is characterized by neurodegeneration and deposition of betaA4, a peptide that is proteolytically released from the amyloid precursor protein (APP). Missense mutations in the genes coding for APP and for the polytopic membrane proteins presenilin (PS) 1 and PS2 have been linked to familial forms of early-onset Alzheimer's disease. Overexpression of presenilins, especially that of PS2, induces increased susceptibility for apoptosis that is even more pronounced in cells expressing presenilin mutants. Additionally, presenilins themselves are targets for activated caspases in apoptotic cells. When we analyzed APP in COS-7 cells overexpressing PS2, we observed proteolytic processing close to the APP carboxyl terminus. Proteolytic conversion was increased in the presence of PS2-I, which encodes one of the known PS2 pathogenic mutations. The same proteolytic processing occurred in cells treated with chemical inducers of apoptosis, suggesting a participation of activated caspases in the carboxyl-terminal truncation of APP. This was confirmed by showing that specific caspase inhibitors blocked the apoptotic conversion of APP. Sequence analysis of the APP cytosolic domain revealed a consensus motif for group III caspases ((IVL)ExD). Mutation of the corresponding Asp664 residue abolished cleavage, thereby identifying APP as a target molecule for caspase-like proteases in the pathways of programmed cellular death.  (+info)

Microvessels from Alzheimer's disease brains kill neurons in vitro. (4/11292)

Understanding the pathogenesis of Alzheimer's disease is of widespread interest because it is an increasingly prevalent disorder that is progressive, fatal, and currently untreatable. The dementia of Alzheimer's disease is caused by neuronal cell death. We demonstrate for the first time that blood vessels isolated from the brains of Alzheimer's disease patients can directly kill neurons in vitro. Either direct co-culture of Alzheimer's disease microvessels with neurons or incubation of cultured neurons with conditioned medium from microvessels results in neuronal cell death. In contrast, vessels from elderly nondemented donors are significantly (P<0.001) less lethal and brain vessels from younger donors are not neurotoxic. Neuronal killing by either direct co-culture with Alzheimer's disease microvessels or conditioned medium is dose- and time-dependent. Neuronal death can occur by either apoptotic or necrotic mechanisms. The microvessel factor is neurospecific, killing primary cortical neurons, cerebellar granule neurons, and differentiated PC-12 cells, but not non-neuronal cell types or undifferentiated PC-12 cells. Appearance of the neurotoxic factor is decreased by blocking microvessel protein synthesis with cycloheximide. The neurotoxic factor is soluble and likely a protein, because its activity is heat labile and trypsin sensitive. These findings implicate a novel mechanism of vascular-mediated neuronal cell death in Alzheimer's disease.  (+info)

Specific regional transcription of apolipoprotein E in human brain neurons. (5/11292)

In central nervous system injury and disease, apolipoprotein E (APOE, gene; apoE, protein) might be involved in neuronal injury and death indirectly through extracellular effects and/or more directly through intracellular effects on neuronal metabolism. Although intracellular effects could clearly be mediated by neuronal uptake of extracellular apoE, recent experiments in injury models in normal rodents and in mice transgenic for the human APOE gene suggest the additional possibility of intraneuronal synthesis. To examine whether APOE might be synthesized by human neurons, we performed in situ hybridization on paraffin-embedded and frozen brain sections from three nondemented controls and five Alzheimer's disease (AD) patients using digoxigenin-labeled antisense and sense cRNA probes to human APOE. Using the antisense APOE probes, we found the expected strong hybridization signal in glial cells as well as a generally fainter signal in selected neurons in cerebral cortex and hippocampus. In hippocampus, many APOE mRNA-containing neurons were observed in sectors CA1 to CA4 and the granule cell layer of the dentate gyrus. In these regions, APOE mRNA containing neurons could be observed adjacent to nonhybridizing neurons of the same cell class. APOE mRNA transcription in neurons is regionally specific. In cerebellar cortex, APOE mRNA was seen only in Bergmann glial cells and scattered astrocytes but not in Purkinje cells or granule cell neurons. ApoE immunocytochemical localization in semi-adjacent sections supported the selectivity of APOE transcription. These results demonstrate the expected result that APOE mRNA is transcribed and expressed in glial cells in human brain. The important new finding is that APOE mRNA is also transcribed and expressed in many neurons in frontal cortex and human hippocampus but not in neurons of cerebellar cortex from the same brains. This regionally specific human APOE gene expression suggests that synthesis of apoE might play a role in regional vulnerability of neurons in AD. These results also provide a direct anatomical context for hypotheses proposing a role for apoE isoforms on neuronal cytoskeletal stability and metabolism.  (+info)

Increased phosphoglycerate kinase in the brains of patients with Down's syndrome but not with Alzheimer's disease. (6/11292)

Impaired glucose metabolism in Down's syndrome (DS) has been well-documented in vivo, although information on the underlying biochemical defect is limited and no biochemical studies on glucose handling enzymes have been carried out in the brain. Through gene hunting in fetal DS brain we found an overexpressed sequence homologous to the phosphoglycerate kinase (PGK) gene. This finding was studied further by investigating the activity levels of this key enzyme of carbohydrate metabolism in the brains of patients with DS. PGK activity was determined in five brain regions of nine patients with DS, nine patients with Alzheimer's disease and 14 controls. PGK activity was significantly elevated in the frontal, occipital and temporal lobe and in the cerebellum of patients with DS. PGK activity in corresponding brain regions of patients with Alzheimer's disease was comparable with controls. We conclude that our findings complement previously published data on impaired brain glucose metabolism in DS evaluated by positron emission tomography in clinical studies. Furthermore, we show that in DS, impaired glucose metabolism, represented by increased PGK activity, is a specific finding rather than a secondary phenomenon simply due to neurodegeneration or atrophy. These observations are also supported by data from subtractive hybridization, showing overexpressed PGK in DS brains at the transcriptional level early in life.  (+info)

Translation of the alzheimer amyloid precursor protein mRNA is up-regulated by interleukin-1 through 5'-untranslated region sequences. (7/11292)

The amyloid precursor protein (APP) has been associated with Alzheimer's disease (AD) because APP is processed into the beta-peptide that accumulates in amyloid plaques, and APP gene mutations can cause early onset AD. Inflammation is also associated with AD as exemplified by increased expression of interleukin-1 (IL-1) in microglia in affected areas of the AD brain. Here we demonstrate that IL-1alpha and IL-1beta increase APP synthesis by up to 6-fold in primary human astrocytes and by 15-fold in human astrocytoma cells without changing the steady-state levels of APP mRNA. A 90-nucleotide sequence in the APP gene 5'-untranslated region (5'-UTR) conferred translational regulation by IL-1alpha and IL-1beta to a chloramphenicol acetyltransferase (CAT) reporter gene. Steady-state levels of transfected APP(5'-UTR)/CAT mRNAs were unchanged, whereas both base-line and IL-1-dependent CAT protein synthesis were increased. This APP mRNA translational enhancer maps from +55 to +144 nucleotides from the 5'-cap site and is homologous to related translational control elements in the 5'-UTR of the light and and heavy ferritin genes. Enhanced translation of APP mRNA provides a mechanism by which IL-1 influences the pathogenesis of AD.  (+info)

Early phenotypic changes in transgenic mice that overexpress different mutants of amyloid precursor protein in brain. (8/11292)

Transgenic mice overexpressing different forms of amyloid precursor protein (APP), i.e. wild type or clinical mutants, displayed an essentially comparable early phenotype in terms of behavior, differential glutamatergic responses, deficits in maintenance of long term potentiation, and premature death. The cognitive impairment, demonstrated in F1 hybrids of the different APP transgenic lines, was significantly different from nontransgenic littermates as early as 3 months of age. Biochemical analysis of secreted and membrane-bound APP, C-terminal "stubs," and Abeta(40) and Abeta(42) peptides in brain indicated that no single intermediate can be responsible for the complex of phenotypic dysfunctions. As expected, the Abeta(42) levels were most prominent in APP/London transgenic mice and correlated directly with the formation of amyloid plaques in older mice of this line. Plaques were associated with immunoreactivity for hyperphosphorylated tau, eventually signaling some form of tau pathology. In conclusion, the different APP transgenic mouse lines studied display cognitive deficits and phenotypic traits early in life that dissociated in time from the formation of amyloid plaques and will be good models for both early and late neuropathological and clinical aspects of Alzheimer's disease.  (+info)

University of California Los Angeles (UCLA) Alzheimers Disease Research Center is one of leading Southern California Alzheimers Disease Research Centers(ADRC). Learn about early signs and symptoms on memory loss and last stages of Alzheimers disease and other dementias through one of the best Alzheimers Neurologists; how to delay the early onset Alzheimers disease and treatments on non-alzheimers dementias such as dementia with Lewy Bodies (DLB), vascular or multi-infarct dementia or frontotemporal dementia (FTD) which is also called Picks disease.
que es el Alzheimer? Alzheimers Disease Research Center at University of California, Los Angles (UCLA) also enrolls patients and subjects in clinical and pre-clinical research program. Alzheimers Disease NeuroImaging Initiative (ADNI) is a brain imaging and biomarkers, and longitudinal studies. We have bilingual staff that speaks Spanish and English. UCLA Alzheimers Disease Research Center is located in Los Angeles, California.
UCLA Alzheimers Disease Research Center at UCLA, Los Angeles, California is looking for clinical trial participants in medication and non-medication research studies for potential drugs to treat Alzheimers disease. Learn the causes, symptoms, risk factors, early onset, progression, treatments, stages related dementias and latest Alzheimers research break-through at the UCLA Alzheimers Disease Research Center.
University of California Los Angeles (UCLA) Alzheimers Disease Research Center is one of the leading Southern California Alzheimers Disease Research Centers(ADRC). Learn about early signs and symptoms on memory loss and Alzheimers disease and other dementias through one of the best Alzheimers Research Centers; how to delay the early onset Alzheimers diesease and treatments on non-alzheimers dementias such as dementia with Lewy Bodies (DLB), vascular or multi-infarct dementia or frontotemporal dementia (FTD) which is also called Picks disease.
New findings in the journal Alzheimers & Dementia: Diagnosis, Assessment & Disease Monitoring may offer new insight into the detection of early-onset Alzheimers disease through changes in the eye.. According to researchers at Johns Hopkins Wilmer Eye Institute, measuring blood flow in the back of the eye might be a route for early detection of the neurodegenerative disease.. For the study, 13 participants were examined. The participants had been diagnosed with an uncommon early-onset Alzheimers disease.. Through optical coherence tomography angiography (OCTA), researchers were able to examine the blood vessels in the back of the eyes of the patients. The disease is known to be marked by mutations established in three separate genes.. From the findings: early-stage (ES) carriers had significantly greater capillary blood flow than controls and late-stage (LS) carriers. ES and LS carriers had significantly greater capillary blood flow heterogeneity than controls. There was no difference between ...
Turic, Dragana, Jehu, Luke, Dunstan, Melanie, Lloyd, Berwyn, Peirce, Tim, Jones, Sue, Hollingworth, Paul, Moore, Pam, Hamilton, Gillian, Busby, Louise V., Walter, Sarah, Archer, Nicola, Foy, Cathrine, Edmondson, Amanda J., Poppe, Michaella, Powell, John, Jones, Lesley, ODonovan, Michael, Lovestone, Simon, Owen, Mike J. and Williams, Julie (2004) P4-090 Evidence of association with late onset Alzheimers disease on chromosome 10Q. Neurobiology of Aging, 25. S500. ISSN 0197-4580 ...
The Michigan Alzheimers Disease Research Center will host its third annual Beyond Amyloid research symposium this summer.. All Michigan Medicine faculty and staff are invited to register for the event, which will take place on Wednesday, June 19 at the MSU College of Human Medicines Seccchia Center, located at 15 Michigan St. NE in Grand Rapids, Michigan.. The keynote speakers include Russel Swerdlow, M.D., director of the University of Kansas Alzheimers Disease Center, and Linda Van Eldik, Ph.D., director of the University of Kentucky Alzheimers Disease Center. Abstracts are also being accepted.. Learn more or register by clicking here.. ...
These findings suggest that the functional neuroanatomical alterations underlying explicit memory changes in mild Alzheimers disease differ from those seen with normal aging. Particularly striking was the fact that the regions showing the greatest decreases in activation in the patients with mild Alzheimers disease compared with the elderly controls were in the hippocampal formation. We hypothesise that this is the result of the extensive neuronal loss (in conjunction with neuritic plaques and neurofibrillary tangles) that develops early in the course of Alzheimers disease.3 It is likely that regional atrophy is also at least partially responsible for the decreased hippocampal activation in Alzheimers disease.16 However, this is unlikely to be the entire explanation for our findings, as we saw little evidence of paradigm linked activation in the hippocampus in six of the seven Alzheimer patients when the MR signal was sampled within a small section of the hippocampus, guided by each ...
HealthDay News) -- Alzheimers patients given sedatives such as Valium or Xanax may have an increased risk for pneumonia, a new study warns.. People with Alzheimers disease are often given these drugs, called benzodiazepines, over the long term, the researchers said.. Examples of benzodiazepines include alprazolam (Xanax), clonazepam (Klonopin), diazepam (Valium), and lorazepam (Ativan).. An increased risk of pneumonia is an important finding to consider in treatment of patients with Alzheimer disease. Pneumonia often leads to admission to hospital, and patients with dementia are at increased risk of death related to pneumonia, Dr. Heidi Taipale, of Kuopio Research Center of Geriatric Care at the University of Eastern Finland, and co-authors wrote.. For the study, the researchers reviewed data from nearly 50,000 Alzheimers patients in Finland. The patients average age was 80 and about two-thirds were women.. The study found that people with Alzheimers who took benzodiazepines were 30 ...
Guided by the latest biomarker and imaging data, scientists have drafted a new set of diagnostic research criteria redefining Alzheimer disease as a condition that develops-and eventually could warrant intervention-decades prior to obvious symptoms. Most clinicians welcomed the changes, which were proposed last month at the International Conference on Alzheimers Disease (ICAD) in Honolulu, Hawaii, but some questioned the benefit of earlier diagnosis while there is yet no way to stop the disease in its tracks (see ARF related news story). Amid this debate looms the critical question of how well biomarkers can predict who among the cognitively normal is heading toward dementia and, eventually, full-blown AD. This report recaps a sampling of ICAD studies that address this issue. By and large, the data suggest that seniors who appear normal on cognitive tests, but nonetheless suspect their memory is off, or who have high brain amyloid or other pathological reads, may already be quietly on the ...
This study was designed to test the interaction between amyloid-β and tau proteins as a determinant of metabolic decline in preclinical Alzheimers disease (AD). We assessed 120 cognitively normal individuals with [|sup|18|/sup|F]florbetapir positron emission tomography (PET) and cerebrospinal fluid …
Authors: Morris, Martha Clare , Evans, Denis A. , Schneider, Julie A. , Tangney, Christine C. , Bienias, Julia L. , Aggarwal, Neelum T. Article Type: Research Article Abstract: Context: It is currently not known whether dietary intakes of folate and vitamins B12 and B6, co-factors in the methylation of homocysteine, protect against Alzheimers disease. Objective: To examine the association between risk of incident Alzheimers disease and dietary intakes of folate, vitamin B-12, and vitamin B-6. Design: Prospective cohort study. Setting: Geographically defined biracial Chicago community. Participants: 1,041 residents, aged 65 years and older, initially free of Alzheimers disease and followed a median 3.9 years for the development of incident disease. Main Outcome Measure: Probable Alzheimers disease identified through …structured clinical neurological evaluation using standardized criteria. Results: A total of 162 persons developed incident Alzheimers disease during follow-up. In logistic ...
TY - JOUR. T1 - Cystatin C - a novel genetic risk factor for late onset alzheimers disease. AU - Crawford, F.. AU - Freeman, M.. AU - Schinka, J.. AU - Morris, M.. AU - Abdullah, L.. AU - Duara, R.. AU - Mulla, M.. PY - 2000/8/7. Y1 - 2000/8/7. N2 - We investigated the occurrence of a Cystatin C genetic variant in 312 Caucasian clinic-based Alzheimers Disease (AD) cases versus 136 age-matched population-based Caucasian controls (age/age of onset range 60-91yrs). Logistic regression analyses revealed a significant 3-way interaction between APO-E e4 genotypes (APO-E4), CST3 G/G genotype and age/age of onset on AD diagnosis (p,.05) suggesting that the genetic risk changes differentially for APO-E or CST3 as a function of age. We stratified our sample based on age/age of onset of 80+yrs versus younger. In the younger group (231 cases; 86 controls) APOE4 conferred significant risk for AD (p,.0001) while CST3 genotype did not (p=.09). In the 80+ group (50 cases; 81 controls) APOE4 no longer ...
Dental health problems in Alzheimers patients can lead to pain, unmanageable behavior and extensive dental treatment. Yet, the dental needs of Alzheimers patients are often overlooked, usually for very understandable reasons: the patients forgetfulness results in unintentional dental neglect; medications may cause chronic dry mouth (reduction in the healthy flow of saliva) that can lead to tooth decay; patients and their families lose contact with their dentist because they are focused on other health issues.. Good dental health can make eating and digesting food easier for an Alzheimers patient, improving the overall quality of life. If you are a caregiver for someone suffering from Alzheimers, here are some tips and techniques from the Alzheimers Association to assist your loved one in maintaining good oral health.. ...
The cognitive profile of Alzheimer patients without (AD E-, n=17) and with (AD, E+, n=15) extrapyramidal signs (rigidity or bradykinesia), at the time of diagnosis, was examined in a 3-year follow-up
A study involving 159 older adults (average age 76) has confirmed that the amount of brain tissue in specific regions is a predictor of Alzheimers disease development. Of the 159 people, 19 were classified as at high risk on the basis of the smaller size of nine small regions previously shown to be vulnerable to Alzheimers), and 24 as low risk. The regions, in order of importance, are the medial temporal, inferior temporal, temporal pole, angular gyrus, superior parietal, superior frontal, inferior frontal cortex, supramarginal gyrus, precuneus.. There was no difference between the three risk groups at the beginning of the study on global cognitive measures (MMSE; Alzheimers Disease Assessment Scale-cognitive subscale; Clinical Dementia Rating-sum of boxes), or in episodic memory. The high-risk group did perform significantly more slowly on the Trail-making test part B, with similar trends on the Digit Symbol and Verbal Fluency tests.. After three years, 125 participants were re-tested. Nine ...
The Alzheimers Disease Research Center (ADRC) at the Icahn School of Medicine at Mount Sinai is a comprehensive research facility and clinical program dedicated to the study and treatment of normal aging and Alzheimers disease.
The identification of mutations in the APP, PS1, and PS2 genes that cause early-onset familial Alzheimers disease (AD), the demonstration that these mutations all increase Abeta42, and the discovery of an association between Apolipoprotein E4 and late-onset Alzheimers disease have dramatically improved our understanding of Alzheimers disease. It is clear, however, that much of the genetic risk in late onset Alzheimers disease remains unexplained. Current strategies to identify other genes that affect late-onset Alzheimers disease have met with limited success often because of the difficulty associated with obtaining late-onset families with sufficient power for reliable linkage analysis. Genetic studies using large numbers of small families or sib-pairs, to increase the power of the analysis, are also currently being performed by several groups however difficulties with the non-replication of positive loci, identified by different studies, has continued. It will also be difficult to ...
The first thing we must bear in mind is that Alzheimers disease isnt a normal part of aging. Thats how Alzheimers differs from Dementia. However, it is fair to say that Alzheimers disease is one of the most common forms of Dementia (70% of all cases). It causes global cognitive deterioration, behavioral disturbances and diffused cortical atrophy associated with neuronal degeneration. Although its prevalence is much higher in the senior population, it is also considered the most frequent form of dementia among those under-65. However, the 65 years mark is merely based on sociological aspects, and it has no biological significance in clinical practice.. What Alice faces is early-onset Alzheimers, a form of the disease that is far rarer than common Alzheimers disease, and often affects people in their prime, regardless of how mentally active they are. This is because early-onset Alzheimers is a genetically conditioned disease, with few environmental factors.. ...
Effect of genetic polymorphisms on Alzheimers disease treatment outcomes: an update Riyadi Sumirtanurdin,1 Amirah Y Thalib,1 Kelvin Cantona,1 Rizky Abdulah1,2 1Department of Pharmacology and Clinical Pharmacy, Faculty of Pharmacy, Universitas Padjadjaran, Jatinangor, Indonesia; 2Center of Excellence in Higher Education for Pharmaceutical Care Innovation, Universitas Padjadjaran, Jatinangor, Indonesia Abstract: Genetic variations in individuals may cause differences in the response to cholinesterase inhibitor drugs used in the treatment of Alzheimers disease (AD). Through this review, we aimed to understand the potential relationship between genetic polymorphisms and treatment response in AD. We conducted a systematic review of the studies published from 2006 to 2018 that assessed the relationship between genetic polymorphisms and the pharmacotherapeutic outcomes of patients with AD. Via several possible mechanisms, genetic polymorphisms of many genes, including ABCA1, ApoE3, CYP2D6, CHAT, CHRNA7, and
The Alzheimers Disease Neuroimaging Initiative (ADNI) unites researchers with study data as they work to define the progression of Alzheimers disease. ADNI researchers collect, validate and utilize data such as MRI and PET images, genetics, cognitive tests, CSF and blood biomarkers as predictors for the disease. Data from the North American ADNIs study participants, including Alzheimers disease patients, mild cognitive impairment subjects and elderly controls, are available from this site.. ...
Calcium: A proven target in the war on Alzheimers disease Alzheimers disease is practically a household word these days, as the number of individuals dia
Naturalhealth365) For the past two decades, researchers have focused on amyloid plaque - deposits typically found in the brains of patients with Alzheimers disease - as both an indicator and a cause of the disease. But, the real problem has become abundantly clear!. In reality, despite years of research (and massive financial backing by Big Pharma), scientists are no closer to a successful method of treatment.. Thomas J. Lewis, PhD - a researcher, author and leading expert on diseases of aging - says he knows the reason for the epic lack of progress on Alzheimers disease, which currently affects 5.7 million Americans. The biggest myth, says Dr. Lewis, is that Alzheimers disease is caused by amyloid plaque.. Several pharmaceutical companies, including GlaxoSmithKline and Johnson and Johnson, have conducted clinical trials on Alzheimers disease patients using anti-amyloid drugs.. These medications are intended to target amyloid plaques, inhibiting their ability to form the neurofibrillary ...
In this study, we have evaluated the levels of blood histamine, serum interleukin-1 beta (IL-1 beta), and plasma tumor necrosis factor-alpha (TNF-alpha) in 20 patients with mild to moderate Alzheimer disease (AD; 13 early onset and 7 late-onset AD subjects) and in 20 age-matched control subjects (C) …
The UW Alzheimers Disease Research Center seeks to advance research in genetic risk, develop neuroimaging biomarkers for preclinical detection, and discover novel treatment strategies, in affiliation with the UW Memory and Brain Wellness Center.
The UW Alzheimers Disease Research Center seeks to advance research in genetic risk, develop neuroimaging biomarkers for preclinical detection, and discover novel treatment strategies, in affiliation with the UW Memory and Brain Wellness Center.
The overall goal of the proposed renewal of the Wisconsin Alzheimers Disease Research Center (Wisconsin ADRC) is to support cutting-edge and innovative researc...
Obstructive sleep apnea (OSA) is much more common in the elderly than in the young; the latest studies show prevalence between 45% and 62% in individuals over 60. It is even higher in patients with dementia such as Alzheimer patients.. Several trials in elderly patients showed modified cognitive functions, particularly executive and attentional functions, in patients with respiratory sleep disorder. However the benefit of CPAP (Continuous Positive Airway Pressure) ventilation for Alzheimer patients is still controversial, as there are few studies documenting its effects on dementia patients cognitive abilities, and clinicians appear reluctant to prescribe this type of treatment.. The investigators must keep in mind that Alzheimer patients suffer significant sleep disorders; advanced- stage patients spend 40% of the night awake and are drowsy a large part of the day. In dementia patients, sleep disorder is a major cause of hospitalization and institutionalization. The prevalence of obstructive ...
Obstructive sleep apnea (OSA) is much more common in the elderly than in the young; the latest studies show prevalence between 45% and 62% in individuals over 60. It is even higher in patients with dementia such as Alzheimer patients.. Several trials in elderly patients showed modified cognitive functions, particularly executive and attentional functions, in patients with respiratory sleep disorder. However the benefit of CPAP (Continuous Positive Airway Pressure) ventilation for Alzheimer patients is still controversial, as there are few studies documenting its effects on dementia patients cognitive abilities, and clinicians appear reluctant to prescribe this type of treatment.. The investigators must keep in mind that Alzheimer patients suffer significant sleep disorders; advanced- stage patients spend 40% of the night awake and are drowsy a large part of the day. In dementia patients, sleep disorder is a major cause of hospitalization and institutionalization. The prevalence of obstructive ...
A bit of peanut butter and a ruler may be an easy way confirm a diagnosis of early-stage Alzheimers disease, U.S. researchers say.
Brussels, Belgium, 19 July 2017 - Today, the Innovative Medicines Initiative (IMI) is launching two new Calls for proposals with topics on Alzheimers disease, big data, vaccines, autoimmune disease, the blood-brain barrier, drug development, and the exploitation of IMI project results. The total budget for the two Calls stands at just over EUR 130 million. Around half of this comes from the European Commissions Horizon 2020 programme. The other half comes from EFPIA companies as well as IMI Associated Partners.
The ε4 allele of apolipoprotein E (ApoE) accounts for an estimated 45-60% of the genetic risk for late onset sporadic Alzheimers disease, suggesting that it may be possible to identify other genetic loci that could account for the remaining risk associated with this disease. Recently, a biallelic polymorphism (G/A) in the 3′ untranslated region (UTR) of the transcription factor LBP-1c/CP2/LSF (for brevity, CP2) has been implicated in Alzheimers disease susceptibility, with the 3′-UTR A allele being associated with a reduction in the risk of sporadic Alzheimers disease.1-3 The CP2 gene is a plausible candidate for influencing Alzheimers disease risk: it is located near the LDL receptor related protein gene within the Alzheimers disease linkage region on chromosome 12; it controls the expression of several genes (α2 macroglobulin, glycogen synthase kinase-3β); and it interacts with different proteins (serum amyloid A3, interleukin 1α, tumour necrosis factor α, and Fe65 protein) and ...
TY - JOUR. T1 - Amyloid β peptide load is correlated with increased β-secretase activity in sporadic Alzheimers disease patients. AU - Li, Rena. AU - Lindholm, Kristina. AU - Yang, Li Bang. AU - Yue, Xu. AU - Citron, Martin. AU - Yan, Riqiang. AU - Beach, Thomas. AU - Sue, Lucia. AU - Sebbagh, Marwan. AU - Cai, Huaibin. AU - Wong, Philip. AU - Price, Donald. AU - Shen, Yong. PY - 2004/3/9. Y1 - 2004/3/9. N2 - Whether elevated β-secretase (BACE) activity is related to plaque formation or amyloid β peptide (Aβ) production in Alzheimers disease (AD) brains remains inconclusive. Here, we report that we used sandwich enzyme-linked immunoabsorbent assay to quantitate various Aβ species in the frontal cortex of AD brains homogenized in 70% formic acid. We found that most of the Aβ species detected in rapidly autopsied brains (,3 h) with sporadic AD were Aβ1-x and Aβ1-42, as well as Aβx-42. To establish a linkage between Aβ levels and BACE, we examined BACE protein, mRNA expression and ...
TY - JOUR. T1 - Healthy lifestyle and the risk of Alzheimer dementia. T2 - Findings from 2 longitudinal studies. AU - Dhana, Klodian. AU - Evans, Denis A.. AU - Rajan, Kumar B.. AU - Bennett, David A.. AU - Morris, Martha C.. PY - 2020/7/28. Y1 - 2020/7/28. N2 - OBJECTIVE: To quantify the impact of a healthy lifestyle on the risk of Alzheimer dementia. METHODS: Using data from the Chicago Health and Aging Project (CHAP; n = 1,845) and the Rush Memory and Aging Project (MAP; n = 920), we defined a healthy lifestyle score on the basis of nonsmoking, ≥150 min/wk moderate/vigorous-intensity physical activity, light to moderate alcohol consumption, high-quality Mediterranean-DASH Diet Intervention for Neurodegenerative Delay diet (upper 40%), and engagement in late-life cognitive activities (upper 40%), giving an overall score ranging from 0 to 5. Cox proportional hazard models were used for each cohort to estimate the hazard ratio (HR) and 95% confidence interval (CI) of the lifestyle score with ...
Mutations at codons 717 and 670/671 in the amyloid precursor protein (APP) are rare genetic causes of familial Alzheimers disease (AD). A mutation at codon 693 of APP has also been described as the genetic defect in hereditary cerebral hemorrhage with amyloidosis of the Dutch type (HCHWA-D). We have reported a APP692Ala--|Gly (Flemish) mutation as a cause of intracerebral hemorrhage and presenile dementia diagnosed as probable AD in a Dutch family. We now describe the post-mortem examination of two demented patients with the APP692 mutation. The neuropathological findings support the diagnosis of AD. Leptomeningial and parenchymal vessels showed extensive deposition of Abeta amyloid protein. Numerous senile plaques consisted of large Abeta amyloid cores, often measuring more than 30 microm in diameter and were surrounded by a fine meshwork of dystrophic neurites. In addition, there were a large number of paired helical filaments in pyramidal neurons and dystrophic neurites. Our findings show that the
TY - JOUR. T1 - Deleterious ABCA7 mutations and transcript rescue mechanisms in early onset Alzheimers disease. AU - De Roeck, Arne. AU - Van den Bossche, Tobi. AU - van der Zee, Julie. AU - Verheijen, Jan. AU - De Coster, Wouter. AU - Van Dongen, Jasper. AU - Dillen, Lubina. AU - Baradaran-Heravi, Yalda. AU - Heeman, Bavo. AU - Sanchez-Valle, Raquel. AU - Lladó, Albert. AU - Nacmias, Benedetta. AU - Sorbi, Sandro. AU - Gelpi, Ellen. AU - Grau-Rivera, Oriol. AU - Gómez-Tortosa, Estrella. AU - Pastor, Pau. AU - Ortega-Cubero, Sara. AU - Pastor, Maria A. AU - Graff, Caroline. AU - Thonberg, Håkan. AU - Benussi, Luisa. AU - Ghidoni, Roberta. AU - Binetti, Giuliano. AU - de Mendonça, Alexandre. AU - Martins, Madalena. AU - Borroni, Barbara. AU - Padovani, Alessandro. AU - Almeida, Maria Rosário. AU - Santana, Isabel. AU - Diehl-Schmid, Janine. AU - Alexopoulos, Panagiotis. AU - Clarimon, Jordi. AU - Lleó, Alberto. AU - Fortea, Juan. AU - Tsolaki, Magda. AU - Koutroumani, Maria. AU - Matěj, ...
Eventbrite - Alzheimers Association, Hudson Valley Chapter presents Alzheimers Disease & Related Disorders Association, Inc. Hudson Valley Chapters 2015 Year End Appeal - Monday, December 7, 2015 | Monday, February 29, 2016 - Find event and ticket information.
Many patients currently diagnosed with very mild or mild Alzheimer disease dementia could potentially be reclassified as having mild cognitive impairment (MCI) under revised criteria for that condition, according to a report published Online First by Archives of Neurology, one of the JAMA/Archives journals.. The National Institute on Aging and the Alzheimers Association convened a work group to update criteria for MCI, and the revised criteria allow considerable latitude as to what represents functional independence, writes the studys sole author, John C. Morris, M.D., of Washington University School of Medicine in St. Louis. For example, mild problems performing daily activities such as shopping, paying bills and cooking are permissible, as is dependency on aids or assistance to complete those tasks.. In this study, the functional ratings of patients enrolled at federally funded Alzheimers Disease Centers with clinical and cognitive data maintained by the National Alzheimers ...
This new book presents a summary of Alzheimers disease-related ischemic protein changes and gene expression as risk factors for the late-onset of sporadic Alzheimers disease, and their role in Alzheimers disease ischemic etiology. Ischemic brain changes were noted in the staining of different parts of an amyloid protein precursor, presenilin 1 and 2, tau protein, alfa-synuclein, and apolipoproteins A1, E and J.. Current advances in understanding the ischemic etiology of Alzheimers disease has revealed dysregulation of Alzheimers disease-associated genes including presenilin 1 and 2, β-secretase, amyloid protein precursor, apoptosis, autophagy, mitophagy, and tau protein. This book presents the relationship between these genes, dysregulated by cerebral ischemia, and the cellular and tissue neuropathology characteristic of Alzheimers disease. This book draws attention to the latest research confirming the theory that Alzheimers disease-related proteins and genes play an important role in ...
The presence of Abeta(pE3) (N-terminal truncated Abeta starting with pyroglutamate) in Alzheimers disease (AD) has received considerable attention since the discovery that this peptide represents a dominant fraction of Abeta peptides in senile plaques of AD brains. This was later confirmed by other reports investigating AD and Downs syndrome postmortem brain tissue. Importantly, Abeta(pE3) has a higher aggregation propensity, and stability, and shows an increased toxicity compared to full-length Abeta. We have recently shown that intraneuronal accumulation of Abeta(pE3) peptides induces a severe neuron loss and an associated neurological phenotype in the TBA2 mouse model for AD. Given the increasing interest in Abeta(pE3), we have generated two novel monoclonal antibodies which were characterized as highly specific for Abeta(pE3) peptides and herein used to analyze plaque deposition in APP/PS1KI mice, an AD model with severe neuron loss and learning deficits. This was compared with the plaque ...
Author(s): Holland, Dominic; Desikan, Rahul S.; Dale, Anders M.; McEvoy, Linda K. | Abstract: Age is the strongest risk factor for sporadic Alzheimer disease (AD), yet the effects of age on rates of clinical decline and brain atrophy in AD have been largely unexplored. Here, we examined longitudinal rates of change as a function of baseline age for measures of clinical decline and structural MRI-based regional brain atrophy, in cohorts of AD, mild cognitive impairment (MCI), and cognitively healthy (HC) individuals aged 65 to 90 years (total n = 723). The effect of age was modeled using mixed effects linear regression. There was pronounced reduction in rates of clinical decline and atrophy with age for AD and MCI individuals, whereas HCs showed increased rates of clinical decline and atrophy with age. This resulted in convergence in rates of change for HCs and patients with advancing age for several measures. Baseline cerebrospinal fluid densities of AD-relevant proteins, Aβ1-42, tau, and phospho
Alzheimers Disease is a progressive neurodegenerative illness characterized by short-term memory loss, disorientation, and impairments in socialization, self-care and behavioral regulation. It is primarily a disease of old age and affects over 5,000,000 Americans. Medications are often prescribed to manage its symptoms, but no medication has been shown to halt or delay the progression of the disease.. Given the enormous personal, social, and economic consequences of this illness, researchers are actively seeking novel ways to slow and forestall its devastating effects.. In a randomized clinical trial, Quintana-Hernández et al. [Journal of Alzheimers Disease] compared the effectiveness of a Mindfulness-Based Alzheimers Stimulation (MBAS) program in maintaining cognitive functioning in Alzheimers patients to that of two current non-pharmacological interventions for Alzheimers disease; namely, Progressive Muscle Relaxation (PMR) and Cognitive Stimulation Therapy (CST).. The researchers ...
Fagan, A. M., Mintun, M. A., Shah, A. R., Aldea, P., Roe, C. M., Mach, R. H., Marcus, D., Morris, J. C. and Holtzman, D. M. (2009), Cerebrospinal fluid tau and ptau181 increase with cortical amyloid deposition in cognitively normal individuals: Implications for future clinical trials of Alzheimers disease. EMBO Mol Med, 1: 371-380. doi: 10.1002/emmm.200900048 ...
BACKGROUND: Knowledge of the evolution of cognitive deficits in Alzheimer disease is important for our understanding of disease progression. Previous reports, however, have either lacked detail or have not covered the presymptomatic stages. OBJECTIVE: To delineate the onset and progression of clinical and neuropsychological abnormalities in familial Alzheimer disease. METHODS: Nineteen subjects with familial Alzheimer disease underwent serial clinical and neuropsychological assessments. Eight of these had undergone presymptomatic assessments. The follow-up period was 1 to 10 years (mean, 5 years). The relative timing of the occurrence of 3 markers of disease onset and progression (onset of symptoms, Mini-Mental State Examination score , or = 24, and impaired scores on a range of neuropsychological tests) were compared using the binomial exact test. RESULTS: Neurological abnormalities were not prominent, although myoclonus appeared early in some. Mini-Mental State Examination score was not ...
Alzheimer Patients can benefit from Ralapure R Alpha Lipoic Acid (R ALA.) Learn how R ALA can exert positive effects in Alzheimer Patients
TY - JOUR. T1 - Gene expression profiles of transcripts in amyloid precursor protein transgenic mice. T2 - Up-regulation of mitochondrial metabolism and apoptotic genes is an early cellular change in Alzheimers disease. AU - Reddy, P. Hemachandra. AU - McWeeney, Shannon. AU - Park, Byung S.. AU - Manczak, Maria. AU - Gutala, Ramana V.. AU - Partovi, Dara. AU - Jung, Youngsin. AU - Yau, Vincent. AU - Searles, Robert. AU - Mori, Motomi. AU - Quinn, Joseph. N1 - Funding Information: The authors thank Sandra Oster, Neurological Sciences Institute, Oregon Health and Science University, for critical reading of the manuscript. This research was supported in part by the Alzheimers Association of Oregon, the Medical Research Foundation of Oregon, the American Federation for Aging Research, a pilot grant from the Alzheimers Disease Center of Oregon, P30 AG08017, and AG22643 (to P.H.R.) and Department of Veterans Affairs Advanced Research Career Development Award and NIH-AT0006 (to J.Q.).. PY - ...
In March of 2016 at the age of 51 I was diagnosed with Younger Onset / Early-Stage Alzheimers Disease. You can read my full story here. Since my diagnosis I have been working with great fervor with the National Alzheimers Association as a member of the National Early-Stage Advisory Group and a Early Stage Ambassador with the Delaware Valley & Greater NJ Early Stage Advisory Councils. The Alzheimers Association has a vision of A world without Alzheimers® and a mission to eliminate Alzheimers disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health.. Please join me in this fight and donate here for the Walk to End Alzheimers.. ...
We examined a deletion/insertion promoter polymorphism of the serotonin transporter gene, which confers an approximately 40% reduction in expression of the protein, in 196 subjects with late onset Alzheimers disease (AD) and 271 controls. The frequency of the 484 bp low activity allele was elevated in the subjects with AD (p = 0.004), and an excess of the low activity genotype (30%) was also found in comparison with the controls (20%) (chi 2 = 7.16; p = 0.03). This association was unrelated to the age of the subjects or controls, or to epsilon 4 alleles of the ApoE gene. The odds ratio for the effect of the homozygous low activity genotype was 1.7 (95% CI 1.08-2.67), with a population attributable risk of 33% (95% CI 5-54%). These findings indicate that the low activity allele of the serotonin transporter is a risk factor for late onset AD.
TY - JOUR. T1 - Neuropsychiatric symptoms as predictors of progression to severe Alzheimers dementia and death. T2 - The cache county dementia progression study. AU - Peters, Matthew E.. AU - Schwartz, Sarah. AU - Han, Dingfen. AU - Rabins, Peter V.. AU - Steinberg, Martin. AU - Tschanz, Joann T.. AU - Lyketsos, Constantine G.. PY - 2015/5/1. Y1 - 2015/5/1. N2 - Objective: Little is known about factors influencing the rate of progression of Alzheimers dementia. Using data from the Cache County Dementia Progression Study, the authors examined the link between clinically significant neuropsychiatric symptoms in mild Alzheimers dementia and progression to severe dementia or death. Method: The Cache County Dementia Progression Study is a longitudinal study of dementia progression in incident cases of this condition. Survival analyses included unadjusted Kaplan-Meier plots and multivariate Cox proportional hazard models. Hazard ratio estimates controlled for age at dementia onset, dementia ...
Supporting: 2, Contrasting: 1, Mentioning: 60 - According to the amyloid theory, the appearance of amyloid-β (Aβ) deposits represents a pivotal event in late onset Alzheimers disease (LOAD). Physiologically, Aβ42 monomers are cleaned by capillary resorption, enzymatic catabolism, and cerebrospinal fluid (CSF) transport. Factors that promote the oligomerization of Aβ42 must be specified. In vitro, these monomers spontaneously form neurotoxic oligomers whose rate increases with time suggesting that the stasis of CSF favors the oligomerization. In animals, experimental hydrocephalus generates CSF stasis followed by the appearance of amyloid deposits. In normal pressure hydrocephalus, amyloid deposits are common, especially in elderly patients, and the turnover decline has the same order of magnitude as in AD. In this disease, the effects of CSF stasis are potentiated by the decline in the ability of CSF to inhibit the formation of oligomers. CSF originates from choroid plexus (CP). In LOAD, the
The second goal was for the gene discovery of the type highlighted in the Nature Genetics article to ultimately contribute to predicting who will develop Alzheimers disease, which will be important when preventive measures become available. Knowing these risk genes will also help identify the first disease-initiating steps that begin in the brain long before any symptoms of memory loss or intellectual decline are apparent. This knowledge will help researchers understand the events that lead to the destruction of large parts of the brain and eventually the complete loss of cognitive abilities. The research published in Nature Genetics was supported by the National Institute on Aging, (part of the National Institutes of Health, which includes 29 Alzheimers Disease Centers), the National Alzheimers Coordinating Center, the NIA Genetics of Alzheimers Disease Data Storage Site, the NIA Late Onset Alzheimers Disease Family Study, and the National Cell Repository for Alzheimers Disease. These ...
Some cases of early-onset Alzheimer disease are caused by gene mutations that can be passed from parent to child. This results in what is known as early-onset familial Alzheimer disease (FAD). Researchers have found that this form of the disorder can result from mutations in the APP, PSEN1, or PSEN2 genes. When any of these genes is altered, large amounts of a toxic protein fragment called amyloid beta peptide are produced in the brain. This peptide can build up in the brain to form clumps called amyloid plaques, which are characteristic of Alzheimer disease. A buildup of toxic amyloid beta peptide and amyloid plaques may lead to the death of nerve cells and the progressive signs and symptoms of this disorder. Other cases of early-onset Alzheimer disease may be associated with changes in different genes, some of which have not been identified.. Some evidence indicates that people with Down syndrome have an increased risk of developing Alzheimer disease. Down syndrome, a condition characterized ...
ALZHEIMERS DISEASE AND RELATED DISORDERS ASSOCIATION offers the opportunity to serve your community through Fundraise with the Alzheimers Association!. This is an ongoing opportunity located in Coral Gables, Florida.
Korean ADNI (K-ADNI) is working to comply with international standards of world-wide ADNI for development of new drugs for Alzheimers Disease dementia patients; to evaluate the effects of vascular risk factors on Alzheimers disease progression and Subcortical Vascular Dementia (SVaD), which comprises relatively large proportion of Asian dementia patients; and to establish the efficacy approval system for new dementia drugs. They are recruiting and collecting data comparable to that gathered through other WW-ADNI centers and data collected throughout this study are available to the research community. Recently, Korea ADNI was approved for government funding.. View more information about Korean ADNI. ...
Variation in the susceptibility to the lethal effects of Alzheimers Amyloid Precursor Protein (APP) transgene exists among various mouse strains. Inbred FVB/N mice, expressing high levels of the transgene-encoded APP, die prior to 200 days, while inbred 129.Tg2576 mice carrying the transgene are far less susceptible. When the two strains are crossed, (FVB/Nxl29.Tg2576) FI mice survive, as does the 129.Tg2576 parent. Intercross and backcross offspring survived at rates of 60% and 35%, respectively, at 200 days signaling the presence of a polygenic trait. The goal of this study was to establish a linkage to genes affecting susceptibility to the APP transgene. The possible quantitative trait loci (QTL) were established using various genetic markers scattered throughout the genome. The presence of multiple QTLs is possible from the data obtained; however, an increased chance of type I errors (false positives) exists due to the large number of markers used for the genome scan ...
OBJECTIVES: To determine if mild cognitive impairment (MCI) represents a continuum of cognitive and functional deficits.. METHODS: Clinical data of 164 subjects with no dementia (ND, n = 52), uncertain dementia (n = 69), and mild probable Alzheimers disease (AD, n = 43) were reviewed. Uncertain dementia patients were classified as pre-MCI (n = 11), early amnestic MCI (e-aMCI, n = 15) and late amnestic MCI (l-aMCI, n = 15). Cognitive assessments [Chinese Mini-Mental State Examination (CMMSE) and a validated neuropsychological battery], functional assessments (Lawtons scale for instrumental activities of daily living) and neuroimaging (ischemic lesions and medial temporal lobe atrophy) were reviewed.. RESULTS: ND, aMCI and mild AD subjects demonstrated a significant trend for worsening performance for all cognitive and functional measures (ANOVA, p , 0.05). Pre-MCI subjects performed significantly better than aMCI subjects in all verbal memory domains (p , 0.001), while l-aMCI had worse ...
Background and Purpose: We sought to assess the efficacy and safety of donepezil in patients with vascular dementia (VaD) fulfilling National Institute of Neurological Disorders and Stroke-Association Internationale pour la Recherche et lEnseignement en Neurosciences criteria.; Methods: This international, multicenter, 24-week trial was conducted from March 2003 to August 2005. Patients (N=974; mean age, 73.0 years) with probable or possible VaD were randomized 2:1 to receive donepezil 5 mg/d or placebo. Coprimary outcome measures were scores on the Vascular-Alzheimer Disease Assessment Scale-Cognitive Subscale and Clinicians Interview-Based Impression of Change, plus carer interview. Analyses were performed for the intent-to-treat population with the last-observation-carried-forward method.; Results: Compared with placebo, donepezil-treated patients showed significant improvement from baseline to end point on the Vascular-Alzheimer Disease Assessment Scale-Cognitive Subscale (least-squares ...
We have developed an ultrasensitive bienzyme-substrate-recycle enzyme-linked immunosorbent assay for the measurement of Alzheimers disease (AD) abnormally hyperphosphorylated tau in cerebrospinal fluid (CSF). The assay, which recognizes attomolar amounts of tau, is approximately 400 and approximately 1300 times more sensitive than conventional enzyme-linked immunosorbent assay in determining the hyperphosphorylated tau and total tau, respectively. With this method, we measured both total tau and tau phosphorylated at Ser-396/Ser-404 in lumbar CSFs from AD and control patients. We found that the total tau was 215 +/- 77 pg/ml in cognitively normal control (n = 56), 234 +/- 92 pg/ml in non-AD neurological (n = 37), 304 +/- 126 pg/ml in vascular dementia (n = 46), and 486 +/- 168 pg/ml (n = 52) in AD patients, respectively. However, a remarkably elevated level in phosphorylated tau was only found in AD (187 +/- 84 pg/ml), as compared with normal controls (54 +/- 33 pg/ml), non-AD (63 +/- 34 pg/ml), and
On November 7th, the Alzheimers Association honored Nashaat Gerges, Ph.D and Joseph Goveas, M.D. during a Research Symposium held at the Medical College of Wisconsin. Dr. William Thies, Chief Medical and Scientific Officer, Alzheimers Association, presented Gerges and Goveas with New Investigator Research Grants for their efforts to advance the understanding of Alzheimers disease, help identify new treatment strategies, provide information to improve care for people with dementia, and further knowledge of brain health and disease prevention. Nashaat Gerges, Ph.D., assistant professor of cell biology, neurobiology and anatomy at the Medical College is receiving the New Investigator Research Grant (NIRG) for his study of the role of retinoic acid in Alzheimers disease. Damage to the brain from oxidative stress occurs in Alzheimers patients. Retinoic acid acts as an antioxidant, and could be useful in reducing that oxidative stress in Alzheimers patients. Dr. Gerges will receive $100,000 over ...
In 31 symptomatic and 5 asymptomatic carriers of the amyloid precursor protein (APP) gene codon 693 mutation, 10 family members without mutation, and 5 carriers of the APP gene codon 692 mutation (3 with early-onset Alzheimer dementia, 2 with cerebral hemorrhage), a high frequency of the apolipoprotein E epsilon 4 allele was found. Age at onset, age at death, occurrence of dementia, and number of strokes did not differ between APP gene mutation carriers with or without epsilon 4 allele, showing that the clinical expression of these APP mutations is not influenced by the apolipoprotein E gene.
July 14, 2010 /Press Release/ -- Researchers at Mount Sinai School of Medicine have used a newly discovered class of biomarkers to investigate the possibility that the shape of brain protein deposits is different in people with Alzheimers who have the highest-risk gene type than in those with the condition who have a neutral risk gene type. The study is being presented July 14 at the 2010 Alzheimers Association International Conference on Alzheimers Disease in Honolulu, Hawaii.. Sam Gandy, MD, PhD, the Mount Sinai Professor in Alzheimers Disease Research, Professor of Neurology and Psychiatry, and Associate Director of the Alzheimers Disease Research Center at Mount Sinai School of Medicine, led the study. Mount Sinai labs led by Patrick R. Hof, MD, Regenstreif Professor of Neuroscience and Vice-Chair for Translational Neuroscience of the Department of Neuroscience and Dara L. Dickstein, PhD, Assistant Professor, Neuroscience also collaborated on the study.. Apolipoprotein E (APOE) is a ...
Type 2 diabetes mellitus has been identified as a risk factor for Alzheimers disease (AD). An impairment of insulin signaling as well as a desensitization of its receptor has been found in AD brains. Glucose-dependent insulinotropic polypeptide (GIP) normalises insulin signaling by facilitating insulin release. GIP directly modulates neurotransmitter release, LTP formation, and protects synapses from the detrimental effects of beta-amyloid fragments on LTP formation, and cell proliferation of progenitor cells in the dentate gyrus. Here we investigate the potential therapeutic property of the new long lasting incretin hormone analogue D-Ala2GIP on key symptoms found in a mouse model of Alzheimer disease (APPswe/PS1detaE9). D-Ala2GIP was injected for 21 days at 25 nmol/kg ip once daily in APP/PS1 male mice and wild type (WT) littermates aged 6 or 12 months of age. Amyloid plaque load, inflammation biomarkers, synaptic plasticity in the brain (LTP), and memory were measured. D-Ala2GIP improved memory in
BACKGROUND/AIMS: Memantine has been approved by the Food and Drug Administration for the treatment of moderate-to-severe Alzheimers disease (AD). However, the effect of memantine on patients with mild-to-moderate AD is unclear. METHODS: This study is a post hoc analysis of a double-blind clinical trial. Donepezil was used as the standard control treatment. Outcomes included score changes from baseline to week 24 on the Alzheimers Disease Assessment Scale-Cognitive Subscale (ADAS-cog), a modified 20-item Activities of Daily Living Scale (ADL), the Neuropsychiatric Inventory (NPI), and the Mini-Mental State Examination (MMSE) as well as the score of the Clinicians Interview-Based Impression of Change plus Caregiver Input (CIBIC-Plus ...
The amyloid cascade hypothesis posits that an extracellular build-up of amyloid-β oligomers (Aβ-os) and polymers (fibrils) subsequently inducing toxic hyperphosphorylated (p)-Tau oligomers (p-Tau-os) and neurofibrillary tangles starts the sporadic late-onset Alzheimers disease (LOAD) in the aged lateral entorhinal cortex. Conversely, mutated genes cause a diffuse cerebral Aβs/Aβ-os overproduction promoting early-onset familiar AD (EOFAD). Surplus exogenous Aβ-os exert toxic actions at several levels. They reach the nuclei of human astrocyte-neurons teams (ANTs) to enhance the transcription of Aβ precursor protein (APP) and β-secretase/BACE1 genes. The overexpressed APP and BACE1 proteins act in concert with γ-secretase to overproduce endogenous Aβs/Aβ-os, of which a few enter the nuclei to upkeep Aβs overproduction, while the rest gather in the cytoplasm, damage mitochondria, and are oversecreted. Simultaneously, extracellular Aβ-os bind the ANTs calcium-sensing receptors (CaSRs) ...
TY - JOUR. T1 - Targeting vascular amyloid in arterioles of alzheimer disease transgenic mice with amyloid β protein antibody-coated nanoparticles. AU - Poduslo, Joseph F.. AU - Hultman, Kristi L.. AU - Curran, Geoffry L.. AU - Preboske, Gregory M.. AU - Chamberlain, Ryan. AU - Marjańska, Małgorzata. AU - Garwood, Michael. AU - Jack, Clifford R.. AU - Wengenack, Thomas M.. PY - 2011/8. Y1 - 2011/8. N2 - The relevance of cerebral amyloid angiopathy (CAA) to the pathogenesis of Alzheimer disease (AD) and dementia in general emphasizes the importance of developing novel targeting approaches for detecting and treating cerebrovascular amyloid (CVA) deposits. We developed a nanoparticle-based technology that uses a monoclonal antibody against fibrillar human amyloid-β42 that is surface coated onto a functionalized phospholipid monolayer. We demonstrate that this conjugated nanoparticle binds to CVA deposits in arterioles of AD transgenic mice (Tg2576) after infusion into the external carotid ...
Mutations in presenilins (PS) 1 and 2 are the major cause of familial Alzheimers disease. Conditional inactivation of PS1 in the mouse postnatal forebrain leads to mild deficits in spatial learning and memory, whereas inactivation of both PS1 and PS2 results in severe memory and synaptic plasticity impairments, followed by progressive and substantial neurodegeneration. Here we investigate the effect of a familial Alzheimers disease-linked PS1 missense mutation using knock-in (KI) mice, in which the wild-type PS1 allele is replaced with the M146V mutant allele. In the Morris water maze task, PS1 KI mice at 3 months of age exhibit reduced quadrant occupancy and platform crossing in the probe trial after 6 days of training, though their performance was normal in the probe trial after 12 days of training. By the age of 9 months, even after 12 days of training, PS1 homozygous KI mice still exhibit reduced platform crossing in the post-training probe trial. ELISA analysis revealed a selective ...
April 23, 2013. Alzheimers disease is a neurodegenerative brain condition that comes with a multibillion-dollar per year cost to the American public, and its takeover doesnt seem to be slowing down. It is estimated that in 2013 alone, Alzheimers disease will cost Americans more than $200 billion. With its prevalence appearing to be at an all time high, it appears that the medical world and the public should be looking for better alternatives in regard to preventing its takeover. The Westernized approach to treating such a condition has some upsides, but many crucial factors seem to be left out of the overall equation - food (like coconuts) being one of these major areas to assess.. The effects of coconut oil on the brain. Coconut oil is an amazing food, and luckily, science has shown that it is among one of the most healing in nature. In regard to helping Alzheimers patients, the ketone bodies, which are given off when coconut oils fatty acids are metabolized by the liver, can be a perfect ...
Dr. Shelanski, a neuropathologist and cell biologist is a pioneer in identifying the major structural elements of the nerve cell and has devoted over 40 years to research on the alterations in nerve cell structure and function in Alzheimers Disease and related dementias. His laboratory has trained a number outstanding researchers in Alzheimers Disease who now lead units at Harvard, Penn and other leading universities. He is the author of over 200 hundred publications in the area of nerve cell biology and cytoskeletal function. Dr. Shelanski has served as Director of the Medical Scientist Training Programs at both NYU and Columbia. He has been a member of review and advisory groups at the National Institutes of Health, the American Cancer Society and a number of private grant makers as well as a member of Scientific Advisory Board and National Board of Directors of the Alzheimers Association. He is the recipient of the 2013 Distinguished Service Award from the University of Chicago Medical ...
The amyloid precursor protein gene (APP) and its derivative peptides have important functions in the central nervous system. APP and Aβ fulfil criteria as neuractive peptides: presence, release and identity of action. Aβ is a peptide of 1 - 43 amino acids in length, derived from APP and the major component of the core of neuritic plaques found in Alzheimers disease. Analysis of the cDNA of Aβ revealed its origins from the larger precursor protein. There are at least four types of mRNA generated by alternative splicing of exons 7 and 8. Exon 7 encodes a 57 amino acid sequence found in the extracellular domain with major homology to the Kunitz-type of serine protease inhibitors. APP is cleaved by three secretases known as α, β, and γ secretase which act on APP at different sites producing various fragments of differing amino acid length. The γ secretase is a macromolecular enzyme complex composed of presenilin 1, 2 and other molecular constitutents essential for its function.
Blood donors of the Madrid area show a 6% frequency of apolipoprotein E genotype carrying allele epsilon 4. This frequency is smaller than other populations of Caucasian origin. This proportion decreases to 4% in a selected sample of healthy individuals of ages | 60 years. The frequency (34%) of the allele epsilon 4 was significantly increased in patients of late onset Alzheimers disease, similarly to other populations. An earlier age of onset of the dementia is observed in the patients of late-onset Alzheimers disease carrying the allele epsilon 4. No increased frequency in allele epsilon 4 frequency was found in patients of early-onset Alzheimers disease. Patients of Parkinsons disease do not show any differences in the frequency of the alleles of apolipoprotein E when compared with healthy individuals.
Study: Ginkgo Improves Lives of Alzheimers Patients & Caregivers Brought to you from the NEEDS Wellness Team A recent published study evaluated the effects of the herb, Ginkgo biloba, on a total of nearly 400 Alzheimers and/or dementia patients. Half of the study group took 120 mg of Ginkgo and the other half took a placebo--both twice daily for 22 weeks. The researchers then measured the patients cognitive state, daily functioning, and severity of neuro-psychiatric symptoms using various testing methods. There was significant improvement in cognitive skills in patients taking the ginkgo, where those taking the placebo experienced cognitive decline. Sixty-one percent of the ginkgo users improved their level of daily living activities (i.e., hygiene, household chores) as compared to an improvement in only 15% of the patients in the placebo group. A larger number of patients in the ginkgo group also experienced a decrease in neuropsychiatric symptoms, including apathy,
Scientists from the Monell Center and the US Department of Agriculture (USDA) alongside other research organizations have been able to differentiate a distinctive odor unique to the urine of Alzheimers patients. The research was however conducted on lab mice models.. Get the Free Tracker App to find a SNES Classic in Stock. The odor signature in the urine of the mice models indicate that potential patients can be diagnosed through the urine odor signature before the manifestation of cognitive symptoms, enabling researchers to develop non-invasive tools for early diagnosis of the disease.. Previous research from the USDA and Monell has focused on body odor changes due to exogenous sources such as viruses or vaccines. Now we have evidence that urinary odor signatures can be altered by changes in the brain characteristic of Alzheimers disease, said study author Bruce Kimball, a chemical ecologist with the USDA National Wildlife Research Center (NWRC) who is stationed at the Monell Center. This ...
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Synaptic dysfunction contributes to cognitive impairment in Alzheimers disease and may be countered by increased intake of nutrients that target brain phospholipid metabolism. In this study, we explored whether the medical food Souvenaid affects brain phospholipid metabolism in patients with Alzheimers disease. Thirty-four drug-naive patients with mild Alzheimers disease (Mini Mental State Examination score ≥20) were enrolled in this exploratory, double-blind, randomized controlled study. Before and after 4-week intervention with Souvenaid or an isocaloric control product, phosphorus and proton magnetic resonance spectroscopy (MRS) was performed to assess surrogate measures of phospholipid synthesis and breakdown (phosphomonoesters [PME] and phosphodiesters [PDEs]), neural integrity (N-acetyl aspartate), gliosis (myo-inositol), and choline metabolism (choline-containing compounds [tCho]). The main outcome parameters were PME and PDE signal intensities and the PME/PDE ratio. MRS data from 33
The deposition of amyloid beta-protein (Abeta) in the vessel wall, i.e., cerebral amyloid angiopathy (CAA), is associated with Alzheimers disease (AD). Two types of CAA can be differentiated by the presence or absence of capillary Abeta-deposits. In addition, as in Alzheimers disease, risk for capillary CAA is associated with the apolipoprotein E (APOE) epsilon4-allele. Because these morphological and genetic differences between the two types of AD-related CAA exist, the question arises as to whether there exist further differences between AD cases with and without capillary CAA and, if so, whether capillary CAA can be employed to distinguish and define specific subtypes of AD. To address this question, we studied AD and control cases both with and without capillary CAA to identify the following: (1) distinguishing neuropathological features; (2) alterations in perivascular protein expression; and (3) genotype-specific associations. More widespread Abeta-plaque pathology was observed in AD ...
AP Science Writer. December 21, 2000 (AP) -- The research was conducted by two independent research teams, centered at the University of South Florida in Tampa and the University of Toronto in Ontario, Canada. The studies used strains of mice that develop lots of amyloid plaques in their brains, along with measurable memory deficits, because of the genes they carry. The researchers used different versions of a procedure in which mice swam until they learned the location of an underwater platform. The animals were then tested to see how well they remembered where the platform was. Alzheimers patients frequently have trouble remembering locations and how to get to destinations.. Both studies found that mice that had been repeatedly vaccinated performed markedly better than the untreated plaque-forming mice in the memory tests. On some occasions they did as well or nearly as well as ordinary mice. University of South Florida researcher Dave Morgan said his vaccinated mice were slower to learn the ...
Disease-modifying treatments in MS are one of the most rapidly evolving areas of therapeutic intervention in neurology. As new treatments become available, the options for patients, and their prescribing physicians, increases. Many of the newer therapies have complex risk: benefit profiles and require specialized expertise for safe and effective administration. Faculty will focus on therapeutic strategies and risk mitigation of currently available disease-modifying therapies, discuss proper use of these drugs and risk assessment, and use specific examples to cover the most frequent issues arising from MS treatment strategies. This program complements C54: Multiple Sclerosis Therapy: Disease-modifying Treatment II and C116: Multiple Sclerosis Therapy: Symptom Management, but covers independent topics ...
Most common neurodegenerative disorders likely result from complex interactions between genetic and environmental risk factors (Farrer et al., 1997; Munoz and Feldman, 2000; Lindsay et al., 2002). One such factor may be aging-related alterations in the redox state of mitochondria (Hirai et al., 2001; Eckert et al., 2003; Beal, 2005) Our study shows that partial reduction in the main mitochondrial superoxide scavenger Sod2 accelerates the onset of hAPP/Aβ-dependent behavioral abnormalities and worsens a range of AD-related molecular and pathological alterations.. How might Sod2 reduction modulate the phenotype of hAPP mice or AD? An obvious mechanism is increased mitochondrial levels of superoxide radicals and resultant oxidative damage. To assess this possibility, we measured mitochondrial aconitase activity, a well-established mitochondrial sensor of superoxide that is lower in the heart and liver of adult Sod2+/− mice than in Sod2+/+ controls (Williams et al., 1998; Van Remmen et al., ...
Loss of intracellular compartmentalization of potassium is a biochemical feature of Alzheimers disease indicating a loss of membrane integrity and mitochondrial dysfunction. We examined potassium and rubidium (a biological proxy for potassium) in brain tissue, blood fractions and cerebrospinal fluid from Alzheimers disease and healthy control subjects to investigate the diagnostic potential of these two metal ions. We found that both potassium and rubidium levels were significantly decreased across all intracellular compartments in the Alzheimers disease brain. Serum from over 1000 participants in the Australian Imaging, Biomarkers and Lifestyle Flagship Study of Ageing (AIBL), showed minor changes according to disease state. Potassium and rubidium levels in erythrocytes and cerebrospinal fluid were not significantly different according to disease state, and rubidium was slightly decreased in Alzheimers disease patients compared to healthy controls. Our data provides evidence that contrasts the
The finding of more than one coexisting brain pathology in dementia sufferers is not unusual. However, it is unclear how these different diseases may interact or influence the evolution of one another. In this study we analyse the hippocampal expression patterns of hyperphosphorylated tau, paired helical filament (PHF)-related protein, beta-amyloid and synaptophysin in a group of Alzheimers disease (AD) sufferers with and without additional pathology. Compared to cases with only AD-type pathology we found that the presence of additional vascular disease augmented the accumulation of hyperphosphorylated tau in the CA1 region of the hippocampus without affecting PHF formation in cases with mild AD changes and reduced the extent of PHF formation in the CA2/3 and CA4 regions of the hippocampus in cases with severe AD pathology. We also found that synaptophysin immunoreactivity in the CA4 and dentate gyrus in pure AD was inversely related to the extent of amyloid accumulation but not to neurofibrillary
10:00am - 3:00pm. This workshop provided education, skills-training, relaxation, and support for caregivers of loved ones with Alzheimers disease or related dementia. Mayo Clinic dementia experts were on hand to answer questions, teach stress management skills, and provide the latest information on dementia care.. ...
In a 2014 scientific study, researchers have discovered strong evidence of the therapeutic effects of THC found in cannabis, in regards to reversing the brain damage associated with Alzheimers Disease. The results clearly are in favor of low-dose, monitored use of cannabis to lower the levels of amyloid-beta precursor proteins, characteristic of this health problem.. Amyloid-beta precursor proteins are large membrane proteins that support neural health, growth, and repair. Due to the natural aging process and the presence of inflammation, a corrupted version of these proteins may begin to produce, destroying neurons and consequently, the memories, thinking process, and even the personality of the Alzheimers patient.. If THC successfully lowers the level of the corrupted amyloid-beta precursor proteins, does this mean that Alzheimers Disease can be completely reversed? Scientists do not yet have clear-cut and straightforward answers to this important question. Even though the political and ...
TY - JOUR. T1 - The Impact of Aging and Alzheimers Disease on Decoding Emotion Cues from Bodily Motion. AU - Insch, Pauline Margaret. AU - Slessor, Gillian. AU - Phillips, Louise Helen. AU - Atkinson, Anthony. AU - Warrington, Jill. N1 - This work was supported by a grant from the Lily Charlton Trust. The authors wish to acknowledge the support of the Older Adult Mental Health Directorate at Royal Cornhill Hospital, NHS Grampian, Alzheimers Scotland and the Scottish Dementia Clinical Research Network. We would also like to thank all the participants for their support in taking part. This project was completed as part of a doctoral dissertation by P. M. Insch.. PY - 2015. Y1 - 2015. N2 - Both healthy aging and dementia cause problems with emotion perception, and the impairment is generally greater for specific emotions (anger, sadness and fear). Most studies to date have focused on static facial photographs of emotions. The current study investigated the effects of healthy aging and Alzheimers ...
UNLABELLED: Transient cognitive and behavioral stabilization of patients with Alzheimers disease (AD) is the main goal of long-term acetylcholinesterase inhibitor (AChEI) therapy, but response to treatment is variable and, indeed, only some of the patients are stabilized. This is usually assessed by means of clinical and neuropsychologic scales, whereas functional neuroimaging could allow objective evaluation of the topographic correlates of the effect of therapy on brain functioning. The aim of this study was to evaluate brain perfusion changes by SPECT in AD patients during chronic AChEI therapy in relation to their cognitive evolution. METHODS: Forty-seven consecutive outpatients with mild-to-moderate probable AD (as defined by the National Institute of Neurological and Communicative Disorders and Stroke-Alzheimers Disease and Related Disorders Association and the Diagnostic and Statistical Manual of Mental Disorders [4th edition criteria] and a score of | or =15 on the Mini-Mental State
The amyloid cascade hypothesis postulates that the initial event which triggers neuronal degradation in Alzheimers disease is enhanced amyloid-β generation and aggregation.
No association of alpha1-antichymotrypsin flanking region polymorphism and Alzheimer disease risk in early- and late-onset Alzheimer disease patients.
APBA2 (amyloid beta precursor protein binding family A member 2), Authors: Dessen P. Published in: Atlas Genet Cytogenet Oncol Haematol.
For the past three decades, research has linked traumatic brain injury with an increased risk of developing Alzheimers disease later in life. According to the Alzheimers Association, research shows that the way traumatic brain injury changes brain chemistry indicates a relationship between traumatic brain injury and hallmark protein abnormalities linked to Alzheimers. Many medications are on the market to treat the condition, but research has shown that occupational therapy can help improve the symptoms of Alzheimers disease as well.. According to HealthDay, many practitioners say occupational therapy can help keep Alzheimers patients safe at home. Occupational therapy consists of a therapist helping a patient, and the patients family, develop treatment plans that help the patient improve with daily activities and occupations. As stated by the The American Occupational Therapy Association, the primary aims of occupational therapy are nhancing function, promoting relationships and social ...
Neuritic plaques and neurofibrillary tangles are crucial morphological criteria for the definite diagnosis of Alzheimers disease. We evaluated 12 unstained frontal cortex and hippocampus samples from 3 brain donors with Alzheimers disease and 1 control with hyperspectral Raman microscopy on samples of 30 × 30 µm. Data matrices of 64 × 64 pixels were used to quantify different tissue components including proteins, lipids, water and beta-sheets for imaging at 0.47 µm spatial resolution. Hierarchical cluster analysis was performed to visualize regions with high Raman spectral similarities. The Raman images of proteins, lipids, water and beta-sheets matched with classical brain morphology. Protein content was 2.0 times, the beta-sheet content 5.6 times and Raman broad-band autofluorescence was 2.4 times higher inside the plaques and tangles than in the surrounding tissue. The lipid content was practically equal inside and outside. Broad-band autofluorescence showed some correlation with ...
Up to five percent of people diagnosed with Alzheimers are in their forties and fifties when it strikes. Known as early-onset Alzheimers, this middle-aged disease affects about 200,000 people in the U.S. alone.
By Alan Fleming People with Alzheimers disease or other dementias pose a unique challenge to first responders. An emergency situation can create an emotionally catastrophic reaction in a person with Alzheimers. Whether they are the person that needs help or a bystander on the scene, people with Alzheimers require special attention. Because they thrive best in a calm and familiar environment, they have considerable difficulty when their routine is disrupted. The Alzheimers Association, West Virginia Chapter offers an interactive training module for first responders, specially created to help them handle emergencies where people with Alzheimers disease or other dementias are present.. The inherent degenerative nature of Alzheimers disease creates a variety of communications challenges. Every person with Alzheimers is different. The disease progresses through different stages with each person exhibiting an array of symptoms and behaviors specific to Alzheimers. How a person with Alzheimers ...
The older African American population is growing at a rapid pace, and the burden of aging-related cognitive impairment and Alzheimers disease will continue to present a tremendous challenge, said Lisa Barnes, PhD. This study highlights the importance of research among minority groups within the communities in which hospitals serve. Barnes is the primary author and director of the Rush Center of Excellence on Disparities in HIV and Aging in the Rush Alzheimers Disease Center, and professor of Neurological Sciences and Behavioral Sciences at Rush University Medical Center. The lack of high-quality biologic data on large numbers of racial and ethnic minorities poses barriers to progress in understanding whether the mechanisms and processes of Alzheimers disease operate the same or differently in racial and ethnic minorities and, if so, how, particularly in the high-risk African American population, said Barnes. In 2010, the U.S. Census Bureau indicated that 20 percent of the population ages ...
  • Alzheimer's disease, a type of dementia, is an irreversible, progressive brain disease that affects an estimated 5.7 million Americans. (cdc.gov)
  • Alzheimer's disease (AD) is the most common form of dementia among older people. (medlineplus.gov)
  • He said of the disease - the most common form of dementia, affecting roughly five million Americans - that, 'I am being treated with medications under the supervision of some of the finest doctors in the field. (newsday.com)
  • Obstructive sleep apnoea (OSA) is a strong risk factor for dementia, both vascular dementia and Alzheimer's disease. (news-medical.net)
  • Osman is a Postdoctoral Research Associate at the University of Sheffield studying the impact of cardiovascular disease (atherosclerosis) on neurovascular function in vascular dementia and Alzheimer's disease using pre-clinical models and neuroimaging techniques. (news-medical.net)
  • "Our data show that while former footballers had higher dementia rates, they had lower rates of death due to other major diseases. (scotsman.com)
  • Alzheimer 's Disease and its History, Symptoms, and Treatments Alzheimer's is a form of dementia and is a progressive mental deterioration that can occur in middle or old age. (ipl.org)
  • More commonly addressed in its chronic form, dementia is associated with a range of diseases such as Alzheimer's Disease, the most common form of dementia (making up to 70% of cases), Parkinson's Disease, vascular dementia, Lewy body dementia, Creutzfeldt-Jakob disease and frontotemporal dementia. (ipl.org)
  • Dementia is a mental process disorder caused by a brain disease (like dementia) or a severe injury to the head. (ipl.org)
  • Dementia is one of the most feared diseases and expensive to society currently. (ipl.org)
  • Alzheimer's disease is the most common cause of dementia, affecting around six in every 10 people with the condition in the UK. (alzheimersresearchuk.org)
  • Despite decades of research, Alzheimer's disease remains a debilitating and eventually fatal dementia with no effective treatment options. (medicalxpress.com)
  • About 560,000 Canadians suffer from some type of dementia (mental deterioration), and more than 60% of these have Alzheimer's disease. (shoppersdrugmart.ca)
  • many conditions that affect the heart and blood vessels (e.g., high blood pressure, high cholesterol, diabetes, obesity) are associated with an increased risk of developing Alzheimer's disease and other types of dementia. (shoppersdrugmart.ca)
  • The blueberry fruit is loaded with healthful antioxidants that could help prevent devastating effects of Alzheimer's disease dementia. (disabled-world.com)
  • The primary efficacy variables were the Clinician's Interview-Based Impression of Change Plus Caregiver Input (CIBIC-Plus) and the Alzheimer's Disease Cooperative Study Activities of Daily Living Inventory modified for severe dementia (ADCS-ADLsev). (unboundmedicine.com)
  • That they seem to be essential for lowering the risk of brain disorders, from the forgetfulness of senior moments to the more serious memory loss and cognitive decline of dementia and Alzheimer's disease, may convince the Franklins of the world that sleep is not for the lazy. (time.com)
  • BioChain's neurological diseased frozen tissue panels are designed for studying Alzheimer, Parkinson's Disease, Dementia, Multiple Sclerosis, Progressive Supranuclear Palsy (PSP), and Depression diseases. (biochain.com)
  • BAN2401-G000-201, a randomized double-blind clinical trial, utilized a Bayesian design with response-adaptive randomization to assess 3 doses across 2 regimens of lecanemab versus placebo in early Alzheimer's disease, mild cognitive impairment due to Alzheimer's disease (AD) and mild AD dementia. (quanterix.com)
  • Alzheimer's disease is the most common cause of Dementia, with over 70 percent of all Dementia cases occurring as a result of Alzheimer's. (momscareplan.com)
  • But, there are different kinds of dementia that are caused by different diseases and disorders of the brain including frontotemporal, Lewy Body, and vascular diseases. (bimari.pk)
  • Differentiating between Alzheimer's disease as well as other types of dementia with respect to clinical presentation and diagnosis could be challenging and could necessitate extensive testing in specialist centers. (bimari.pk)
  • Researchers have realized that a lot of these conditions and diseases may co-exist in the brain and combine to trigger the development of dementia. (bimari.pk)
  • In the United States, the cost of providing care for people suffering from Alzheimer's disease and other forms of dementia is estimated to be 203 billion dollars in 2013. (bimari.pk)
  • It is the most common type of dementia (a group of diseases which results in memory impairment). (yourchennai.com)
  • There are nearly 55 million people affected with dementia all over the world and nearly 70-80% of them have been diagnosed with Alzheimer's disease. (yourchennai.com)
  • Alzheimer's disease, the most common type o f dementia , is becoming more prevalent as the average life expectancy continues to increase. (lcbseniorliving.com)
  • Alzheimer's disease is the most common type of dementia. (thehealthfact.com)
  • Other kinds of dementia include Huntington's disease, Parkinson's disease, and Creutzfeldt-Jakob disease. (thehealthfact.com)
  • Dementia only appears when our brains are impaired by neurodegenerative diseases. (kcl.ac.uk)
  • The most known neurodegenerative diseases include Alzheimer's Disease, Frontotemporal Dementia and Amyotrophic Lateral Sclerosis. (kcl.ac.uk)
  • There are still no effective treatments for the neurodegenerative diseases that cause dementia, and many questions remain as to the root causes. (kcl.ac.uk)
  • The UK Dementia Research Institute (UK DRI) is the single biggest investment the UK has ever made in neurodegenerative diseases, thanks to £290 million from founding funders the Medical Research Council (MRC), Alzheimer's Society and Alzheimer's Research UK. (kcl.ac.uk)
  • Our major disease interest is on Amyotrophic Lateral Sclerosis (ALS), Frontotemporal Dementia (FTD) and Alzheimer's Disease (AD). (kcl.ac.uk)
  • Alzheimer's disease (AD) is the most frequent form of neurodegenerative disorder associated with dementia in the elderly. (lidsen.com)
  • We are looking at an example of the usefulness of multidisciplinary research to tackle diseases as complex and devastating as dementia. (healthwnews.com)
  • Multiple neuropathologic processes may underlie dementia, including both neurodegenerative diseases and vascular disease. (medscape.com)
  • 2] All dementia share common molecular mechanisms responsible for disease etiology and progression, such as hypoxia and oxidative stress, neuroinflammation, mitochondrial bioenergetics, neurodegeneration, and blood-brain barrier permeability. (medscape.com)
  • Alzheimer disease (AD) is the most common neurodegenerative disease responsible for dementia. (medscape.com)
  • Alzheimer's disease is a progressive form of dementia that affects nearly 6.5 million people in the United States. (cdc.gov)
  • Alzheimer's disease is the most prevalent form of dementia that affects elderly people and it is defined as a progressive and persistent loss of multiple areas of intellectual functions. (bvsalud.org)
  • Alzheimer's disease is the most common cause of dementia, which contributes to a decline in memory, thinking, and social. (medlineplus.gov)
  • Alzheimer's disease (AD) is a neurodegenerative disorder which is characterized by increasing dementia. (mbexc.de)
  • Alzheimer's disease (AD), the most common form of dementia worldwide, is estimated to make up 50-80% of all cases. (ucl.ac.uk)
  • We hypothesized that periodontitis would be associated with increased dementia severity and a more rapid cognitive decline in Alzheimer's disease . (bvsalud.org)
  • We aimed to determine if periodontitis in Alzheimer's disease is associated with both increased dementia severity and cognitive decline , and an increased systemic pro inflammatory state . (bvsalud.org)
  • In 1998 Alzheimer's disease ranked 12th among leading causes of death but jumped to 8th in 1999, due mainly to the inclusion of a cause of death formerly classified separately as "presenile dementia," which accounted for a substantial number of additional Alzheimer's deaths in 1999. (cdc.gov)
  • The presentation of degenerative disease in focal areas of the cerebral cortex is the hallmark of the family of diseases referred to as frontotemporal dementia (also termed frontotemporal lobar degeneration). (medscape.com)
  • There have been a number of rumors and some press reaching out to me,' the Brooklyn-born Lawrence, 83, said in a statement to Newsday through his representative, Howard Bragman, 'and I feel it's important that I tell my own truth: I have been diagnosed with Alzheimer's disease, and it's in the early stages. (newsday.com)
  • Tony was diagnosed with Alzheimer's disease in 2015, and Josie followed a year later. (denverpost.com)
  • For example, if an individual had undergone a serious accident and had head trauma, this could play an important role in being diagnosed with Alzheimer's disease. (ipl.org)
  • Tony Bennett has been diagnosed with Alzheimer's disease - but it hasn't quieted his legendary voice.The singer's wife and son revealed in the latest edition of AARP The Magazine that Bennett was first diagnosed with the irreversible neurological disorder in 2016. (wbaltv.com)
  • Tony Bennett has been diagnosed with Alzheimer's disease - but it hasn't quieted his legendary voice. (wbaltv.com)
  • What are the most important things individuals recently diagnosed with Alzheimer's disease should know? (agingresearch.org)
  • This forgetfulness progressed until, eventually, she was diagnosed with Alzheimer's Disease. (dragoosoilblends.com)
  • Centers for Disease Control and Prevention. (cdc.gov)
  • U.S. Department of Health and Human Services, Public Health Service, Centers for Disease Control and Prevention, National Institute for Occupational Safety and Health, Division of Surveillance, Hazard Evaluation and Field Studies, Surveillance Branch. (cdc.gov)
  • The opinions expressed by authors contributing to this journal do not necessarily reflect the opinions of the U.S. Department of Health and Human Services, the Public Health Service, the Centers for Disease Control and Prevention, or the authors' affiliated institutions. (cdc.gov)
  • The Centers for Disease Control and Prevention (CDC) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. (cdc.gov)
  • The Centers for Disease Control and Prevention (CDC) cannot attest to the accuracy of a non-federal website. (cdc.gov)
  • I'm Commander Ibad Khan, and I'm representing the Clinician Outreach and Communication Activity, COCA, with the Emergency Risk Communication Branch at the Centers for Disease Control and Prevention. (cdc.gov)
  • Neuroinflammation has been known to play a critical role in the pathogenesis of chronic neurodegenerative disease in general, and in AD in particular. (nih.gov)
  • Led by consultant neuropathologist Dr Willie Stewart, honorary clinical associate Professor at the University of Glasgow, the FIELD study found that former professional footballers had an approximately three and a half times higher rate of death due to neurodegenerative disease than expected. (scotsman.com)
  • Dr Stewart, said: "This is the largest study to date looking in this detail at the incidence of neurodegenerative disease in any sport, not just professional footballers. (scotsman.com)
  • A strength of our study design is that we could look in detail at rates of different neurodegenerative disease subtypes. (scotsman.com)
  • Although footballers had higher risk of death from neurodegenerative disease, they were less likely to die of other common diseases, such as heart disease and some cancers, including lung cancer. (scotsman.com)
  • As such, whilst every effort must be made to identify the factors contributing to the increased risk of neurodegenerative disease to allow this risk to be reduced, there are also wider potential health benefits of playing football to be considered. (scotsman.com)
  • The association between contact sport participation and neurodegenerative disease has been subject to debate in recent years. (scotsman.com)
  • However, until this study, it was not clear whether there was any evidence of an increase in neurodegenerative disease rate in former footballers. (scotsman.com)
  • Rod Petrie, Scottish FA President: "We welcome the findings of this important study - the most comprehensive one ever commissioned into neurodegenerative disease in former professional footballers anywhere in the world. (scotsman.com)
  • Our study clearly demonstrates that these non-replicating cells are going through the deterioration process of senescence and that it is directly related to neuroinflammation and Alzheimer's disease," says co-corresponding author and Professor Rusty Gage, president of the Salk Institute and holder of the Vi and John Adler Chair for Research on Age-Related Neurodegenerative Disease. (medicalxpress.com)
  • Alzheimer''s disease is a progressive neurodegenerative disease affecting memory and thinking and making the person increasingly dependent on others. (medindia.net)
  • Experts in the field of Alzheimer's are especially excited, since there are currently no treatments for the neurodegenerative disease, and sleep-based strategies might open new ways to slow its progression in some and even prevent it in others. (time.com)
  • At the cellular level, which proteins in the human body are affected by neurodegenerative disease - what are the causes and consequences? (kcl.ac.uk)
  • Can we use gene therapy to prevent or half the progression of neurodegenerative disease, and can we improve the way they are delivered? (kcl.ac.uk)
  • Her research focuses on medical genetics and stem cell modeling to unlock disease mechanisms and pathways leading to neurodegeneration in Parkinson's disease and related disorders, and to develop new therapeutic strategies to advance precision medicine. (stanford.edu)
  • During her neurology internship from 2001 to 2002 at Medical University of Lübeck with Prof. Christine Klein, Dr. Schüle studied genes for inherited forms of Parkinson's disease and dystonia. (stanford.edu)
  • He is a senior anatomic neuropathologist with considerable experience in the evaluation and assessment of Alzheimer's disease, Parkinson's disease and other neurodegenerative disorders. (stanford.edu)
  • This analysis revealed that risk ranged from a 5-fold increase in Alzheimer's disease, through an approximately 4 fold increase in motor neurone disease, to a 2 fold Parkinson's disease in former professional footballers compared to population controls. (scotsman.com)
  • Dr. Horn added that DBS is best understood in Parkinson's disease, "where a noise signature in a specific frequency band can be observed in a specific circuit in the brain. (beyondfitnessforever.com)
  • Over the last seven years, we have created a detailed map of the epigenetic alterations that occur in the brain of people affected by Alzheimer's and other dementias such as those associated with the so-called Lewy bodies or Parkinson's disease. (healthwnews.com)
  • FDA approves aducanumab to treat Alzheimer's disease June 07, 2021, 05:38 p.m. (mayoclinic.org)
  • Mayo researchers, collaborators identify 'instigator' gene associated with Alzheimer's disease April 19, 2021, 03:00 p.m. (mayoclinic.org)
  • It is important to note that not all large-scale studies have shown a significant correlation between sleep disruption and Alzheimer's disease, either in the pre-clinical stage or after symptoms develop. (news-medical.net)
  • Because the disease develops later in life a patient will die before symptoms become severe. (ipl.org)
  • There are also many symptoms of Alzheimer 's. (ipl.org)
  • The trial involved 891 people who already had mild or moderate symptoms of Alzheimer's disease. (newscientist.com)
  • If further tests confirm that taking LMTX on its own really does slow the progression of the disease, this would suggest that tau tangles might be the main cause of Alzheimer's symptoms instead. (newscientist.com)
  • About 5% of people with the disease get symptoms in their 30s, 40s, or 50s. (webmd.com)
  • While certain treatments can help against Alzheimer's symptoms, "there's no current way to stop or slow" the disease itself, says Heather M. Snyder, PhD, of the Alzheimer's Association. (webmd.com)
  • Johns Hopkins researchers say that by measuring levels of certain proteins in cerebrospinal fluid (CSF), they can predict when people will develop the cognitive impairment associated with Alzheimer's disease years before the first symptoms of memory loss appear. (hopkinsmedicine.org)
  • But it has been hard to see Alzheimer's disease coming, even though we believe it begins developing in the brain a decade or more before the onset of symptoms," she adds. (hopkinsmedicine.org)
  • One of the most recognizable symptoms of Alzheimer's disease is a speech problem, such as a person choosing the wrong words, or not understanding simple sentences. (shoppersdrugmart.ca)
  • Depressive symptoms are common in patients with Alzheimer's disease. (medscape.com)
  • In 2005, the FDA added a black box warning on the use of all atypical (second-generation) antipsychotic agents in the treatment of secondary symptoms of Alzheimer's disease, such as agitated or aggressive behavior. (medscape.com)
  • Over 90% of those suffering from this disease, the symptoms do appear after 60. (bimari.pk)
  • Researchers from Charité - Universitätsmedizin Berlin have discovered DBS helps lessen symptoms in people with Alzheimer's disease. (beyondfitnessforever.com)
  • In a recent study, researchers from Charité - Universitätsmedizin Berlin found that DBS may help reduce symptoms in people with Alzheimer's disease (AD). (beyondfitnessforever.com)
  • The electrodes create electric pulses that interrupt abnormal signals the brain may receive, causing symptoms of a disease such as tremors or movement difficulties. (beyondfitnessforever.com)
  • Certainly Alzheimer's disease involves a substantial loss of the elements of the cholinergic system and it is generally accepted that the symptoms of Alzheimer's disease are related to this cholinergic deficit, particularly in the cerebral cortex and other areas of the brain. (pharmaapis.com)
  • Common symptoms of Alzheimer's disease include memory loss, language problems, and impulsive or unpredictable behavior. (thehealthfact.com)
  • But people with Alzheimer's disease exhibit some ongoing behaviors and symptoms that worsen over time. (thehealthfact.com)
  • Symptoms change according to the stage of the disease. (thehealthfact.com)
  • Alzheimer's is a progressive disease, which means that symptoms will progressively deteriorate over the long run. (thehealthfact.com)
  • At present, the US Food and Drug Administration has not approved any psychotropic agent for the treatment of Alzheimer's disease. (medscape.com)
  • Learn more about the treatment of Alzheimer's disease. (medscape.com)
  • Its main therapeutic use is in the palliative treatment of Alzheimer's disease. (pharmaapis.com)
  • Its main therapeutic use is in the treatment of Alzheimer's disease where it is used to increase cortical acetylcholine. (pharmaapis.com)
  • Recent studies have shown that lack of sleep, for even one night, can significantly increase levels of beta-amyloid in the brain - one of the main toxic proteins that are linked to Alzheimer's disease. (news-medical.net)
  • Researchers found that during MRI scans, personalized music activated regions in the brain typically spared from Alzheimer's disease. (aarp.org)
  • What they found during MRI scans is that personalized music, as opposed to background music or similar rhythms, activated regions in the brain typically spared from Alzheimer's disease and that the "functional connectivity" continued even after the music was played. (aarp.org)
  • This may not be the pattern of sleep seen in patients with Alzheimer's disease and other neurodegenerative conditions, however. (news-medical.net)
  • Previously, a phase 2b trial showed no significant difference between lecanemab and placebo at 12 months in patients with Alzheimer's disease. (physiciansweekly.com)
  • According to some studies, depression is present in up to 50% of patients with Alzheimer's disease, the onset of which typically occurs prior to the clinical diagnosis of Alzheimer's disease. (medscape.com)
  • Results of several studies indicate that anticonvulsants (eg, gabapentin, valproic acid ) may have a role in the treatment of behavioral problems in patients with Alzheimer's disease. (medscape.com)
  • 2. The precise mechanism of action of donepezil in patients with Alzheimer's disease is not fully understood. (pharmaapis.com)
  • The known genetics of early- and late-onset Alzheimer's disease are reviewed, including APOE, which is a complex disorder with environmental and genetic components leading to disease. (semanticscholar.org)
  • Researchers probing the complexities of Alzheimer's disease have detected issues involving cellular energy production, and those problems may be an important contributor to the late-onset form of the illness. (harvard.edu)
  • Alois Alzheimer, gave information on a 51-year-old woman who underwent a brain disorder. (ipl.org)
  • Although most caregivers of persons with Alzheimer's disease are women, male caregivers are equally at risk for strain during long term caregiving. (utoledo.edu)
  • What are some common difficulties faced by caregivers of individuals with Alzheimer's disease? (agingresearch.org)
  • Alzheimer's disease can be very demanding and overwhelming for caregivers. (agingresearch.org)
  • Neurocognitive decline with aging and in conditions such as Alzheimer's disease represents a substantial public health concern that will produce suffering in patients and caregivers and enormous expenditures of health care resources. (disabled-world.com)
  • To help those who are dealing with Alzheimer's today, we have launched a targeted awareness campaign to help people with Alzheimer's and their caregivers find resources that can help them manage the disease. (archives.gov)
  • Antiglutamatergic treatment reduced clinical deterioration in moderate-to-severe Alzheimer's disease, a phase associated with distress for patients and burden on caregivers, for which other treatments are not available. (unboundmedicine.com)
  • In order to understand the economic and personal impact of Alzheimer's disease and its related dementias on people suffering from the disease family members and caregivers as well as the federal and state governments, figures on Alzheimer's disease and related diseases are included in the state-wide plan. (bimari.pk)
  • WASHINGTON - The FDA approved aducanumab, a drug for treating Alzheimer's disease, Monday under its Accelerated Approval Program. (wtsp.com)
  • According to Biogen, aducanumab removes the amyloid-beta peptide-protein from an Alzheimer's patient's brain, which has shown in clinical trials to reduce the clinical decline of the disease. (wtsp.com)
  • Cite this: Fast Five Quiz: Test Your Knowledge on Key Aspects of Alzheimer's Disease - Medscape - Feb 09, 2023. (medscape.com)
  • We have found a very high prevalence of OSA in the World Trade Center responder population, and the present work will evaluate the impact of OSA on early markers of Alzheimer 's Disease using plasma biomarkers, PET/MR and cognition using a visual-spatial memory test. (cdc.gov)
  • In this review, we investigate and describe both well-established and recently discovered AD biomarkers that could potentially be used to detect AD at early stages and allow the monitoring of disease progression. (ucl.ac.uk)
  • In addition, we explore the most recent molecular strategies for an AD therapeutic approach and nanomedicine-based technologies, used to both target drugs to the brain and serve as devices for tracking disease progression diagnostic biomarkers. (ucl.ac.uk)
  • What Are the Signs of Alzheimer's Disease? (medlineplus.gov)
  • Padilla notes that because this recent research was an observational study, the findings don't actually prove that high blood pressure caused the signs of Alzheimer's disease. (healthline.com)
  • Blueberries and strawberries have a major role to play in keeping your brain functioning at its best and may help slow down signs of Alzheimer's disease. (hindustantimes.com)
  • Memory problems are one of the first warning signs of Alzheimer's disease and related dementias, and people with the disease can eventually lose the ability to carry on a conversation and respond to the environment. (cdc.gov)
  • The causes of Alzheimer's disease and other dementias are not completely understood, but researchers believe they include a combination of genetic, environmental, and lifestyle factors. (cdc.gov)
  • The causes of Alzheimer's disease aren't fully understood, however, researchers believe that they are a result of a mix of environmental, genetic, or lifestyle variables. (bimari.pk)
  • These methods allowed her group to understand how some brains cells are vulnerable to the impact of Alzheimer's disease while others are resilient. (agingresearch.org)
  • The person with Alzheimer's disease must rely on others to assist in the most basic tasks of daily life including eating. (bimari.pk)
  • The caregiver plays an important role in the management of person with Alzheimer's disease along with the help of other family members. (yourchennai.com)
  • Ultimately, a person with Alzheimer's disease may require full-time support. (thehealthfact.com)
  • New computational model proposed for Alzheimer's disease March 28, 2022, 03:30 p.m. (mayoclinic.org)
  • Learn how Alzheimer's disease affects the brain. (alz.org)
  • They contribute anonymous autopsy data to the National Alzheimer Coordinating Center , and prepare a brain autopsy report for a participant's next of kin. (stanford.edu)
  • She is currently applying single-cell methods to human brain to dissect the contributions of distinct cell types to Alzheimer's disease pathogenesis and investigate the mechanisms of tau-mediated neurodegeneration in human brain. (stanford.edu)
  • More recently, progressive degenerative brain disease (chronic traumatic encephalopathy [CTE] has been recognized in athletes with a history of multiple concussions, as well as milder blows to the head that do not cause concussion. (medscape.com)
  • Music has long been thought to soothe the soul, but a new study published in The Journal of Prevention of Alzheimer's Disease shows how personalized music playlists can activate regions of the brain typically untouched by early Alzheimer's disease and may offer a new way to approach anxiety, depression and agitation in patients. (aarp.org)
  • The two have five children, and worry which of the siblings might also develop the degenerative brain disease. (denverpost.com)
  • Alzheimer's disease is a brain disorder that slowly degrades a person's memory and thinking skills. (denverpost.com)
  • The scientists, led by Lukas Kunz of the German Centre for Neurodegenerative Diseases in Bonn, say the high risk group navigated the maze differently and had reduced functioning of a type of brain cell involved in spatial navigation. (bbc.com)
  • She added: 'Although we don't know whether the young people in this study will go on to develop Alzheimer's, characterising early brain changes associated with genetic risk factors is important to help researchers better understand why some people may be more susceptible to the disease later in life. (bbc.com)
  • Improving Brain Health for Populations Disproportionately Affected by Alzheimer's Disease and Related Dementias. (cdc.gov)
  • This is pertinent to Anatomy and Physiology because Alzheimer's disease leads to tissue loss and nerve cell damage throughout the brain. (ipl.org)
  • Alzheimer's Disease impacts an individual's memory and other vital brain functions. (ipl.org)
  • Although it's not confirmed scientist believe for most people, Alzheimer's disease results from a combination of genetic, life styles and environmental factors that affect the brain over time. (ipl.org)
  • The trial was the first major test of a drug that targets tau tangles - abnormal protein clumps that accumulate and spread in the brains of people with Alzheimer's disease, disrupting brain function. (newscientist.com)
  • It also contains the preservative thimerosal, a derivative of mercury, a known neurotoxin linked to brain damage and autoimmune diseases. (rense.com)
  • People with genetic forms are more likely to go on to develop the disease and will have the hallmark features such as amyloid protein build-up which damages our brain cells. (alzheimersresearchuk.org)
  • Her expertise in looking at how brain cells connect and communicate can then be used with this new model to understand how different cells in the brain react to amyloid build-up, and what processes are disrupted at different points in Alzheimer's disease. (alzheimersresearchuk.org)
  • Her work has the potential to unlock the cascade of events in the brain that cause Alzheimer's and create a new model to better understand and ultimately treat the disease in the future. (alzheimersresearchuk.org)
  • Unlike the mild memory loss that can happen with aging, Alzheimer's disease takes a growing toll on the brain . (webmd.com)
  • Now, new research suggests that hypertension can also seriously affect your brain - perhaps to the point of developing some of the primary markers of Alzheimer's disease. (healthline.com)
  • The Gage team found that senescent neurons are a source of the late-life brain inflammation observed in Alzheimer's disease. (medicalxpress.com)
  • More work still needs to be conducted on how senescent neurons lead to Alzheimer's disease as well as the consequences of removing these neurons from the brain. (medicalxpress.com)
  • We also contributed to research in the journal, Science , describing how brain function in Alzheimer's disease is altered at the level of neurons in later stages of the disease. (agingresearch.org)
  • Those who already have the disease do better if they keep mentally active - an unused brain may deteriorate faster. (shoppersdrugmart.ca)
  • some scientists speculate that prions , tiny infectious particles made of protein, may be involved in Alzheimer's disease by infecting the brain. (shoppersdrugmart.ca)
  • Eating certain foods can slow brain ageing and reduce the chances of developing Alzheimer's disease. (hindustantimes.com)
  • Here's expert-approved diet to keep this brain disease at bay. (hindustantimes.com)
  • Alzheimer's disease , a neurological disorder, can make your brain shrink or brain cells die over the period of time. (hindustantimes.com)
  • Alzheimer's disease (AD) is a devastating disease of the aging population characterized by the progressive and slow brain decay due to the formation of extracellular plaques in the hippocampus. (frontiersin.org)
  • Furthermore, the emerging nanomedicines for managing brain diseases like AD could promote the booming growth of research and their clinical availability. (frontiersin.org)
  • peptide, which makes up the characteristic brain plaques of Alzheimer's disease, is not secreted by neurons from mice that lack the BACE1 secretase. (the-scientist.com)
  • Overall, this study found that in persons with early Alzheimer's disease, lecanemab was associated with reduced brain amyloid levels as well as moderately less decline in clinical measures of cognition and function than placebo at 18 months. (physiciansweekly.com)
  • Alzheimer's is a particular brain disease that was first identified over 100 years ago, however the research into its causes, the risk factors, and possible treatments only started to gain momentum over the past 30 years. (bimari.pk)
  • The most prominent signs of this disease are the buildup of abnormal brain proteins such as clumps of beta-amyloid (called amyloid plaques) and tangled bundles of tau filaments (called neurofibrillary knots). (bimari.pk)
  • The swelling caused by a byproduct of amyloid plaques in the brain may be the true cause of Alzheimer's disease, say researchers. (androidizer.com)
  • The formation of amyloid plaques in the brain is a hallmark of Alzheimer's disease . (androidizer.com)
  • Alzheimer's Disease (AD) is a slow and progressive brain disorder which results in the gradual worsening of memory and thinking skills, eventually resulting in an inability to do even simple things over time. (yourchennai.com)
  • These changes initially involve the nerve cells in the brain which are responsible for memory and learning, but as the disease progresses it will involve other parts of the brain. (yourchennai.com)
  • It is a focal stimulation that needs to be targeted to a specific brain structure in each disease. (beyondfitnessforever.com)
  • In Alzheimer's disease, nerve cells and brain tissue are destroyed and the brain shrinks significantly over the course of several years causing a progressive loss of memory. (dragoosoilblends.com)
  • Swelling and oxidative stress cause and contribute to several biological processes in the body which lead to the destruction of brain tissue and Alzheimer's Disease. (dragoosoilblends.com)
  • Alzheimer's disease is a condition that affects the brain. (thehealthfact.com)
  • These diseases cause a loss of functions in brain cells. (kcl.ac.uk)
  • Our research looks at the similarities and differences between these diseases to find the keys to slow or halt loss of brain cells at the earliest stages. (kcl.ac.uk)
  • How does disease affect the functions of brain cells such as the communication between neurons or the structural integrity of the neurons? (kcl.ac.uk)
  • Recent research has shown that posttraumatic amnesia and chronic vascular lesions caused by traumatic brain injury (TBI) increase risk for subsequent Alzheimer's disease. (medscape.com)
  • Quitting smoking now may help maintain brain health and can reduce your risk of heart disease, cancer, lung disease, and other smoking-related illnesses. (cdc.gov)
  • Our goal is to understand the structural and functional properties of excitable cells in the heart and brain across multiple length scales in order to decipher disease-relevant, nanoscale functional units in heart and nerve cells. (mbexc.de)
  • His case study "On the relationship between aphasia and senile atrophy of the brain" still serves as a frame of reference for apparently focal brain syndromes in diffuse or generalized degenerative diseases of the brain. (medscape.com)
  • The National Center for Chronic Disease Prevention and Health Promotion (NCCDPHP) works in four key areas or domains: epidemiology and surveillance, environmental approaches, health care system interventions, and community programs linked to clinical services. (cdc.gov)
  • With $4.5 million in FY 2018 funding, CDC's Alzheimer's Disease and Healthy Aging Program supports these efforts by focusing its activities in two of NCCDPHP's four domains: epidemiology and surveillance and community programs linked to clinical services. (cdc.gov)
  • Read more about Mayo Clinic Alzheimer's disease clinical trials opportunities here . (mayoclinic.org)
  • A drug that has failed in a large clinical trial may still show promise for halting the progression of Alzheimer's disease. (newscientist.com)
  • So it was possible to tell at what stage they progressed from this mild cognitive impairment stage to the clinical Alzheimer's disease stage. (cosmosmagazine.com)
  • Studies that have predicted conversion from mild cognitive impairment to Alzheimer's disease have not really focused on a time frame, and for use in a clinical setting, this is what is really needed. (cosmosmagazine.com)
  • The drug is the first treatment that could potentially reduce the 'clinical decline' of those who have the disease. (wtsp.com)
  • The primary endpoint was Bayesian analysis of 12-month clinical change on the Alzheimer's Disease Composite Score (ADCOMS) for the ED90 dose, which required an 80% probability of ≥25% clinical reduction in decline versus placebo. (quanterix.com)
  • Although distinct in the areas of the nervous system affected, these diseases do share common clinical pathological features. (kcl.ac.uk)
  • OBM Geriatrics is an Open Access journal published quarterly online by LIDSEN Publishing Inc. The journal takes the premise that innovative approaches - including gene therapy, cell therapy, and epigenetic modulation - will result in clinical interventions that alter the fundamental pathology and the clinical course of age-related human diseases. (lidsen.com)
  • With the changing emphasis from genetic to epigenetic understandings of pathology (including telomere biology), with the use of gene delivery systems (including viral delivery systems), and with the use of cell-based therapies (including stem cell therapies), a fatalistic view of age-related disease is no longer a reasonable clinical default nor an appropriate clinical research paradigm. (lidsen.com)
  • whoever possesses the variation has a greater probability of suffering from Alzheimer's disease, so people carrying these variants could be excellent candidates for clinical prevention trials of the disease in the future," adds Esteller. (healthwnews.com)
  • 14, 15, 16] Cholinesterase inhibitors, approved for Alzheimer disease, are sometimes used in this condition, but there is no evidence that FTD involves a cholinergic deficit, and there is no clinical evidence of benefit. (medscape.com)
  • Targeting senescent cells could thus be a useful approach for slowing neuroinflammation and neurodegeneration in Alzheimer's disease. (medicalxpress.com)
  • This study has the potential to identify the mechanisms by which sleep disruption contributes to Alzheimer's Disease neurodegeneration and guide therapeutic interventions in the future in the aging WTC responder population. (cdc.gov)
  • Eli Lilly and Company pain and neurodegeneration vice-president Mark Mintun said: "We are extremely pleased about these positive findings for donanemab as a potential therapy for people living with Alzheimer's disease, the only leading cause of death without a treatment that slows disease progression. (clinicaltrialsarena.com)
  • Previous research links neurodegeneration of the fornix to Alzheimer's disease. (beyondfitnessforever.com)
  • Several studies have shown that the APOE gene, the best-known genetic risk factor for Alzheimer's disease, may have a stronger association with neurodegeneration in women, which could be due how the gene interacts with estrogen. (lcbseniorliving.com)
  • Modifiable risk factors for Alzheimer disease and related dementias among adults aged ≥ 45 years-United States, 2019. (cdc.gov)
  • In support of research on Alzheimer disease and related disorders, the Neuropathology Core analyzes tissues and other biological samples from volunteers in the Stanford Alzheimer's Disease Research Center (ADRC). (stanford.edu)
  • Some chronic sleep disorders can also increase the risk of Alzheimer's disease. (news-medical.net)
  • Alzheimer disease and associated disorders / Western Geriatric Research Institute. (bvs.br)
  • Definition of neurology: a science involved in the study of the nervous systems, especially of the diseases and disorders affecting them. (neurosciencenews.com)
  • Her research program combines her background in diagnostic neuropathology, knowledge of developmental neuroscience, and state-of-the-art cellular and molecular technologies to advance the understanding of Alzheimer's disease and related dementias. (stanford.edu)
  • Helping to promote awareness of Alzheimer's disease and other dementias, including the importance of early diagnosis. (cdc.gov)
  • One of the reasons we sleep, it now seems, might be to keep a range of illnesses-including cognitive diseases like Alzheimer's and other dementias-at bay. (time.com)
  • Alzheimer's disease is among numerous dementias. (bimari.pk)
  • The phrase "Alzheimer's disease and related dementias" is often used to describe it and its related neurodegenerative conditions. (bimari.pk)
  • HHS Emphasizes Healthy Aging to Delay Onset of Alzheimer's disease and Related Dementias. (cdc.gov)
  • Did you know that Black and Latino adults are at much higher risk of Alzheimer's disease and related dementias (ADRD) than White adults? (cdc.gov)
  • On Friday (Jan 6), the US Food and Drink Administration (FDA) granted a licence for another anti-amyloid drug - lecanemab - to treat Alzheimer's disease. (outsourcing-pharma.com)
  • They also explored senescence markers and gene expression of post-mortem brains from 20 people with Alzheimer's disease and matched healthy controls. (medicalxpress.com)
  • This dance between viral particles and cellular APP results in changes in cellular architecture and the distribution of APP, the major component of senile plaques found in the brains of Alzheimer's disease patients. (medindia.net)
  • But when that process fails, misfolded proteins can form the gummy amyloid plaques often found in the brains of Alzheimer's patients. (medicalnewstoday.com)
  • Most patients with Alzheimer's develop sleep problems which worsen as the disease progresses. (news-medical.net)
  • While this is a valuable approach for many research questions, animals can't perfectly replicate how the disease develops and progresses in people. (alzheimersresearchuk.org)
  • Each case of Alzheimer's usually affects at least two lives: the person with the condition, and the patient's spouse or child who gradually becomes a full-time caregiver as the disease progresses. (shoppersdrugmart.ca)
  • Periodontitis is common in the elderly and may become more common in Alzheimer's disease because of a reduced ability to take care of oral hygiene as the disease progresses. (bvsalud.org)
  • Corticotropin-Releasing Factor Receptor 1 Activation During Exposure to Novelty Stress Protects Against Alzheimer's Disease-Like Cognitive Decline in AßPP/PS1 Mice , Journal of Alzheimer's Disease. (alz.org)
  • Re-activation and growth of HSV1 infections contribute to cognitive decline associated with Alzheimer's disease. (medindia.net)
  • Researches and studies reveal that consuming a Mediterranean diet can majorly reduce the risk of decline from cognitive impairment and Alzheimer's disease. (hindustantimes.com)
  • Such a malfunction, he said, could damage or kill nerve cells and help explain the cognitive decline associated with the disease. (harvard.edu)
  • Overall, this study demonstrates that lecanemab was associated with reduced markers of amyloid in early Alzheimer's disease and resulted in less decline in cognitive and functional measures than placebo at 18 months but was associated with significant adverse effects. (physiciansweekly.com)
  • However, a trial of 313 patients with moderate Alzheimer's disease found that 24 months of treatment with valproate did not delay emergence of agitation or psychosis, did not slow cognitive or functional decline, and was associated with significant toxic effects. (medscape.com)
  • Eli Lilly and Company has reported that data from Phase II TRAILBLAZER-ALZ study of its investigational antibody, donanemab, showed a significant slowing of decline in patients with early symptomatic Alzheimer's disease. (clinicaltrialsarena.com)
  • Donanemab showed significant slowing of decline in patients with early symptomatic Alzheimer's disease. (clinicaltrialsarena.com)
  • Data from the trial showed that donanemab slowed decline by 32% versus placebo, thereby meeting the primary endpoint of change from baseline to 76 weeks in the Integrated Alzheimer's Disease Rating Scale (iADRS). (clinicaltrialsarena.com)
  • Can exercise slow or prevent cognitive decline in older people who are at increased risk for Alzheimer's disease? (medlineplus.gov)
  • Periodontitis and Cognitive Decline in Alzheimer's Disease. (bvsalud.org)
  • Elsewhere raised serum pro-inflammatory cytokines have been associated with an increased rate of cognitive decline in Alzheimer's disease . (bvsalud.org)
  • Our data showed that periodontitis is associated with an increase in cognitive decline in Alzheimer's Disease , independent to baseline cognitive state , which may be mediated through effects on systemic inflammation . (bvsalud.org)
  • Apparently, their research indicated that individuals who receive annual flu vaccines were likely to demonstrate a 17% lower prevalence of Alzheimer's disease. (ileanaberman.com)
  • The expansion in the prevalence of this disease due to the increase in life expectancy is a worldwide socioeconomic challenge. (lidsen.com)
  • early-onset Alzheimer's disease has a higher prevalence of TBI . (medscape.com)
  • Researchers at Mayo Clinic study Alzheimer's disease, mild cognitive impairment , and other conditions that affect your memory and thinking skills. (mayoclinic.org)
  • Also watch Dr. Petersen discuss a Mayo Clinic mild cognitive impairment study and a Mayo Clinic study regarding the most effective methods to predict Alzheimer's disease on YouTube. (mayoclinic.org)
  • The tool revolves around examining mild cognitive impairment (MCI), which is often a precursor to Alzheimer's disease. (cosmosmagazine.com)
  • We used data from the Alzheimer's Disease Neuroimaging Initiative [a US-based longitudinal study], and we focused only on people who had mild cognitive impairments, for many years, with multiple assessments. (cosmosmagazine.com)
  • One study involved 47 adults aged 68 and older, who had mild cognitive impairment , a risk condition for Alzheimer's disease. (disabled-world.com)
  • The present study furthered the research by analyzing data from electrodes implanted in the same area of the fornix in 46 people with mild Alzheimer's disease. (beyondfitnessforever.com)
  • In a six month observational cohort study 60 community dwelling participants with mild to moderate Alzheimer's Disease were cognitively assessed and a blood sample taken for systemic inflammatory markers. (bvsalud.org)
  • These conditions occur for patients with severe disease but also for patients who had mild or even asymptomatic acute infection. (cdc.gov)
  • The study has limitations, though, says Lisa Barnes , a cognitive neuropsychologist at the Rush Alzheimer's Disease Center in Chicago, who wrote an accompanying editorial. (tpr.org)
  • Nevertheless, these findings are significant, as they demonstrate that lecanemab may provide cognitive and functional benefits in patients with early Alzheimer's disease. (physiciansweekly.com)
  • Researchers study risk factors, predictors, diagnostic techniques, and potential treatments for Alzheimer's disease and other conditions. (mayoclinic.org)
  • Researchers sometimes work to better understand Alzheimer's by studying animals bred to develop specific features of the disease. (alzheimersresearchuk.org)
  • Researchers have known that these proteins were in the spinal fluid of patients with advanced disease. (hopkinsmedicine.org)
  • The researchers also discovered that targeting the deteriorating neurons with therapeutics could be an effective strategy for preventing or treating Alzheimer's disease. (medicalxpress.com)
  • A method by Rice University researchers to model the way proteins fold - and sometimes misfold - has revealed branching behavior that may have implications for Alzheimer's and other aggregation diseases. (medicalnewstoday.com)
  • The researchers say PLD3 may be used as a marker in diagnosing the risk of Alzheimer's disease and provide a target for future therapies. (androidizer.com)
  • Phase 3 clinicial trial results show that this treatment can meaningfully change the course of the disease for people in the earliest stages of Alzheimer's disease. (alz.org)
  • ntly, findings were published in the Journal of Alzheimer's Disease that may help explain why people who are susceptible to stress are at more risk of developing Alzheimer's and why - increasingly - we are finding evidence that physical activity, which reduces stress levels, may reduce the chances of developing Alzheimer's . (alz.org)
  • Interestingly, previous studies have shown that people with Alzheimer's disease have a reduced level of CRF. (alz.org)
  • Advocacy organisation, Voices of Alzheimer's, (VOA) is led by people with lived experience of the disease. (outsourcing-pharma.com)
  • Dr Laura Phipps of Alzheimer's Research , said the latest study focused on healthy younger people at higher genetic risk of Alzheimer's, suggesting they may already show alterations in spatial navigation several decades before the disease could start. (bbc.com)
  • This incurable, degenerative, and terminal disease is usually diagnosed in people over 65 years of age, although the less-prevalent early-onset AD can occur much earlier. (springer.com)
  • In the United States, more than five million people are currently living with Alzheimer's disease (Marsa). (ipl.org)
  • People often wonder, where did Alzheimer 's get its name from? (ipl.org)
  • In this pilot project, Dr Afia Ali will lead her team in developing the technique needed to successfully grow stem cells from people living with rare genetic forms of Alzheimer's disease. (alzheimersresearchuk.org)
  • Most people with Alzheimer 's are 65 and older. (webmd.com)
  • Dealing with Alzheimer's disease can take a toll on people emotionally and financially. (kunm.org)
  • Now, scientists from the Salk Institute have found that neurons from people with Alzheimer's disease show deterioration and undergo a late-life stress process called senescence. (medicalxpress.com)
  • In this study, Gage and his team took skin samples from people with Alzheimer's disease and converted those cells directly into neurons in the lab. (medicalxpress.com)
  • In the later stages, people with Alzheimer's disease begin to have trouble caring for themselves and recognizing friends or loved ones. (shoppersdrugmart.ca)
  • For instance, people viewing substances are generally most interested in viewing diseases that these substances have shown to have positive influences. (greenmedinfo.com)
  • Scientists don't yet fully understand what causes Alzheimer's disease in most people. (hindustantimes.com)
  • The number of people with Alzheimer's disease doubles about every 5 years beyond age 65. (hindustantimes.com)
  • About one-third of all people age 85 and older may have Alzheimer's disease," says the NIA report. (hindustantimes.com)
  • Alzheimer's Disease is the sixth leading cause of death in the United States killing more people than breast cancer and prostate cancer combined. (pbs.org)
  • This is a truly national plan, based on a strong partnership with every part of the Alzheimer's community, including scientists, patient advocates, and people living with the disease. (archives.gov)
  • These steps in research and education are the cornerstones of an ambitious and aggressive agenda to improve the lives of people living with Alzheimer's disease and their families. (archives.gov)
  • Up to 5% of people diagnosed with Alzheimer's are under age 65-usually in their 40s or 50s-and are considered to have Early-Onset Alzheimer's disease. (momscareplan.com)
  • If all people suffering from Alzheimer's disease in Illinois resided in one city this would be the second-largest city in the state. (bimari.pk)
  • Your gift could help fund the researcher who finds the cure for Alzheimer's disease once and for all. (brightfocus.org)
  • Currently there is no permanent cure for Alzheimer's disease anywhere in the world. (yourchennai.com)
  • The aim of this study is to use classification methods to predict future onset of Alzheimer's disease in cognitively normal subjects through automated linguistic analysis. (thelancet.com)
  • What May Prevent or Delay the Onset of Alzheimer's Disease? (bimari.pk)
  • To gather and assess information on Alzheimer's disease and its treatment from published studies to depict the overall treatment effect, a thorough understanding of the disease's natural history was able to develop appropriate trial designs and outcomes for the various stages of Alzheimer's disease. (semanticscholar.org)
  • When they used gene therapy to remove PLD3 from neurons in mice with a condition resembling Alzheimer's disease, they found that this led to a dramatic reduction of axonal swelling. (androidizer.com)
  • The finding "implies that the biological mechanisms underlying Alzheimer's disease may be very different in [different] racial groups," says Dr. John Morris , an author of the paper and director of the Knight Alzheimer's Disease Research Center at Washington University in St. Louis. (tpr.org)
  • Here, it is described as the use of simple animal models such as worms, fishes, flies, Ascidians and sea urchins, have facilitated the understanding of several biochemical mechanisms underlying Alzheimer's disease (AD), one of the most diffuse neurodegenerative pathologies. (springer.com)
  • What Do We Know about Diet and Prevention of Alzheimer's Disease? (medlineplus.gov)
  • The progression of Alzheimer's disease can be divided into 3 stages. (yourchennai.com)
  • Depression is an important consideration in the differential diagnosis of Alzheimer disease (AD). (medscape.com)
  • According to the amyloid hypothesis cascade, the beta-amyloid (Aβ) peptide deposits are the fundamental cause of the disease [ 1 ]. (springer.com)
  • 1. Lecanemab was associated with reduced amyloid markers in early Alzheimer's disease as compared to placebo. (physiciansweekly.com)
  • Evaluation of neurological effects of cerium dioxide nanoparticles doped with different amounts of zirconium following inhalation exposure in mouse models of Alzheimer's and vascular disease. (openrepository.com)
  • The incidence of the disease increases with age and doubles every 5 years beyond age 65. (cdc.gov)
  • Aluminum is another flu vaccine ingredient and is also a toxic heavy metal that has been associated with an increased incidence of Alzheimer's Disease. (rense.com)
  • Incidence of Alzheimer's disease in a rural community in India: the Indo-US study. (greenmedinfo.com)
  • The incidence of the disease is increasing as you age. (bimari.pk)
  • The Considerable Toll of HZO Is Also Avoidable Dr Christopher Rapuano explains how the rising incidence of this debilitating eye disease can be combated by ophthalmologists and other clinicians. (medscape.com)
  • He is based in the Department of Infection, Immunity & Cardiovascular Disease in the Faculty of Medicine at Sheffield. (news-medical.net)
  • It is now increasingly accepted that sleep loss may indeed be an important risk factor and symptom of Alzheimer's disease. (news-medical.net)
  • An example of a symptom of Alzheimer 's disease(AD) is memory loss. (ipl.org)
  • Fast Five Quiz: Alzheimer's Disease - Medscape - May 06, 2022. (medscape.com)
  • In particular, model organisms are widely used to explore potential causes and treatments for human disease when human experimentation would be unfeasible or unethical. (springer.com)
  • Myth No. 4: There are treatments that stop the disease from getting worse. (webmd.com)
  • No evidence shows they're useful treatments for the disease. (webmd.com)
  • Early treatments keep heart disease patients from getting worse, and it's possible the same may be true for those with pre-symptomatic Alzheimer's," says Marilyn Albert, Ph.D., a professor of neurology at the Johns Hopkins University School of Medicine. (hopkinsmedicine.org)
  • Alzheimer's disease is not a normal part of aging, and scientists are working to understand its causes and develop effective treatments. (cdc.gov)
  • This holiday season, your donation gives help and hope to the millions of families facing Alzheimer's - while also advancing critical research to end the disease. (alz.org)
  • His research interests include mitochondrial diseases, nerve and muscle pathology, pediatric neuro-oncology, and transgenic mouse pathology. (stanford.edu)
  • Specifically, the program provides data and resources to practitioners in the areas of healthy aging and Alzheimer's disease prevention and awareness, supports applied public health research, and helps national organizations share information and tools with the aging population. (cdc.gov)
  • Our results could provide a new basic framework for preclinical research on Alzheimer's disease and may provide a neurocognitive explanation of spatial disorientation in Alzheimer's disease,' they report in Science. (bbc.com)
  • The risk factors for Alzheimer's are diverse, including age, genetics and lifestyle, and research is vital to allow us to unpick how each of these factors could contribute to a person's risk of the disease. (bbc.com)
  • A key priority in Alzheimer's disease (AD) research is the identification of early intervention strategies that will decrease the risk, delay the onset, or slow the progression of disease. (thelancet.com)
  • Read more about the focus of Alzheimer's disease research at Mayo Clinic here . (mayoclinic.org)
  • The Mayo Clinic Alzheimer's Disease Research Center is jointly based in Rochester, Minnesota, and Jacksonville, Florida. (mayoclinic.org)
  • Science Saturday: In neurodegenerative diseases, Mayo Clinic research finds shared gene patterns, widespread damage May 28, 2022, 11:00 a.m. (mayoclinic.org)
  • Some research suggests it might be related to health conditions like heart disease, high blood pressure, and diabetes. (webmd.com)
  • In honor of National Alzheimer's Disease Awareness Month, the Alliance for Aging Research is spotlighting BrightFocus Foundation, a member of the ACT-AD coalition. (agingresearch.org)
  • BrightFocus funds exceptional scientific research worldwide to defeat Alzheimer's disease, macular degeneration, and glaucoma and provides expert information on these heartbreaking diseases. (agingresearch.org)
  • What is the goal of the BrightFocus Alzheimer's Disease Research Program? (agingresearch.org)
  • What are some recent notable findings from Alzheimer's disease research sponsored by BrightFocus? (agingresearch.org)
  • BrightFocus research funding is also being used to support new discoveries about how the processes that cells use to destroy misfolded proteins, like the ones that create plaques and tangles, can go wrong in Alzheimer's disease (described in Neuroscience letters in April). (agingresearch.org)
  • Your tax-deductible gift to Alzheimer's Disease Research will go TWICE as far today. (brightfocus.org)
  • By providing your email address, you will receive periodic communications from Alzheimer's Disease Research. (brightfocus.org)
  • As Guest Editor for this Special Issue of the journal OBM Geriatrics, it is my pleasure to invite you to submit a feature article, which may be either a review or a research paper, on the topic of Oxidative Stress and Alzheimer's Disease. (lidsen.com)

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