Alzheimer Disease: 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)Amyloid beta-Peptides: 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.tau Proteins: 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).Amyloid beta-Protein Precursor: 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.Neurofibrillary Tangles: 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.Plaque, Amyloid: Accumulations of extracellularly deposited AMYLOID FIBRILS within tissues.Brain: 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.Apolipoprotein E4: 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.Amyloid Precursor Protein Secretases: 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.Cognition Disorders: Disturbances in mental processes related to learning, thinking, reasoning, and judgment.Dementia: 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.Presenilin-1: 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.Amyloid: 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.Atrophy: 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.Dementia, Vascular: 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)Neuropsychological Tests: 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.Neurofibrils: 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.Mild Cognitive Impairment: 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.Apolipoproteins E: 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.Presenilin-2: 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.Peptide Fragments: Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.Mental Status Schedule: Standardized clinical interview used to assess current psychopathology by scaling patient responses to the questions.Hippocampus: 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.Cognition: Intellectual or mental process whereby an organism obtains knowledge.Magnetic Resonance Imaging: 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.Lewy Body Disease: 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)Memantine: AMANTADINE derivative that has some dopaminergic effects. It has been proposed as an antiparkinson agent.Age of Onset: 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.Presenilins: 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.Aging: The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.Aspartic Acid Endopeptidases: A sub-subclass of endopeptidases that depend on an ASPARTIC ACID residue for their activity.Aniline CompoundsNeurons: 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.Cholinesterase Inhibitors: 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.Mice, Transgenic: Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.National Institute on Aging (U.S.): 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.Substantia Innominata: 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.Memory Disorders: 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.Cerebral Cortex: 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.Cerebral Amyloid Angiopathy: 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)Longitudinal Studies: Studies in which variables relating to an individual or group of individuals are assessed over a period of time.Amyloidogenic Proteins: 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.Autopsy: Postmortem examination of the body.Brain Chemistry: 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.Positron-Emission Tomography: 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.Disease Progression: 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.Nerve Degeneration: 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.Protease Nexins: Extracellular protease inhibitors that are secreted from FIBROBLASTS. They form a covalent complex with SERINE PROTEASES and can mediate their cellular internalization and degradation.Prodromal Symptoms: Clinical or physiological indicators that precede the onset of disease.Phenylcarbamates: 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.Disease Models, Animal: 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.Tauopathies: 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.Neurodegenerative Diseases: 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.Indans: Aryl CYCLOPENTANES that are a reduced (protonated) form of INDENES.Nootropic Agents: 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.Down Syndrome: 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)Genetic Predisposition to Disease: A latent susceptibility to disease at the genetic level, which may be activated under certain conditions.Lewy Bodies: 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.Clioquinol: 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.ThiazolesFrontotemporal Dementia: 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.Biological Markers: 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.Amnesia: 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)Genotype: The genetic constitution of the individual, comprising the ALLELES present at each GENETIC LOCUS.Temporal Lobe: 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.Psychomotor Agitation: A feeling of restlessness associated with increased motor activity. This may occur as a manifestation of nervous system drug toxicity or other conditions.Nerve Tissue ProteinsNeuropil Threads: 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.Case-Control Studies: 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.Cohort Studies: 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.Insulysin: 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 3.4.24.56.Apolipoprotein E3: 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.Tacrine: 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.Memory: 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.Chromosomes, Human, Pair 21: A specific pair of GROUP G CHROMOSOMES of the human chromosome classification.Monomeric Clathrin Assembly Proteins: A subclass of clathrin assembly proteins that occur as monomers.Phosphorylation: The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.Reference Values: 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.Parkinson Disease: 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)Mutation: 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.Apolipoprotein E2: 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.Kluver-Bucy Syndrome: 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.Galantamine: 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.Risk Factors: 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.Frontotemporal Lobar Degeneration: 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.Benzothiazoles: Compounds with a benzene ring fused to a thiazole ring.Genetic Testing: 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.Neurocalcin: A neuronal calcium sensor protein that is expressed as several isoforms and can interact with ACTIN; TUBULIN; and CLATHRIN.Amyloidosis: 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.LDL-Receptor Related Proteins: A family of proteins that share sequence similarity with the low density lipoprotein receptor (RECEPTORS, LDL).CA2 Region, Hippocampal: A subsection of the hippocampus, described by Lorente de No, that is located between the HIPPOCAMPUS CA1 FIELD and the HIPPOCAMPUS CA3 FIELD.Nerve Fibers, Myelinated: 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.Alleles: Variant forms of the same gene, occupying the same locus on homologous CHROMOSOMES, and governing the variants in production of the same gene product.Glycogen Synthase Kinase 3: 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.Caregivers: 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.Severity of Illness Index: Levels within a diagnostic group which are established by various measurement criteria applied to the seriousness of a patient's disorder.Cyclin-Dependent Kinase 5: 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.Postmortem Changes: Physiological changes that occur in bodies after death.Models, Biological: 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.Entorhinal Cortex: 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.Dominican Republic: 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)Frontal Lobe: The part of the cerebral hemisphere anterior to the central sulcus, and anterior and superior to the lateral sulcus.Clusterin: 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.Psychiatric Status Rating Scales: Standardized procedures utilizing rating scales or interview schedules carried out by health personnel for evaluating the degree of mental illness.Molecular Sequence Data: 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 Factors: 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.Image Processing, Computer-Assisted: 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.Microglia: 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.Oxidative Stress: 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).Amino Acid Sequence: 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.PC12 Cells: 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.Astrocytes: 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.Polymorphism, Single Nucleotide: A single nucleotide variation in a genetic sequence that occurs at appreciable frequency in the population.Maze Learning: 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)Caribbean Region: 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.Protein Binding: 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.Immunohistochemistry: Histochemical localization of immunoreactive substances using labeled antibodies as reagents.Aluminum: A metallic element that has the atomic number 13, atomic symbol Al, and atomic weight 26.98.PrPC Proteins: 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.Caspase 6: 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.Microtubule-Associated Proteins: 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.Alzheimer Vaccines: Vaccines or candidate vaccines used to prevent or treat ALZHEIMER DISEASE.Gene Frequency: The proportion of one particular in the total of all ALLELES for one genetic locus in a breeding POPULATION.Membrane Proteins: 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.Gliosis: The production of a dense fibrous network of neuroglia; includes astrocytosis, which is a proliferation of astrocytes in the area of a degenerative lesion.Reproducibility of Results: 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.Neurofilament Proteins: 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)Aphasia, Primary Progressive: 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)Prions: 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.Lemur: 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.Fluorodeoxyglucose F18: 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)Family Health: 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.Protein Multimerization: The assembly of the QUATERNARY PROTEIN STRUCTURE of multimeric proteins (MULTIPROTEIN COMPLEXES) from their composite PROTEIN SUBUNITS.Cerebral Ventricles: 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).Predictive Value of Tests: 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.Solubility: 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)Protein Structure, Tertiary: 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.Proteolysis: 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, Cultured: 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.Time Factors: Elements of limited time intervals, contributing to particular results or situations.Parahippocampal Gyrus: A convolution on the inferior surface of each cerebral hemisphere, lying between the hippocampal and collateral sulci.Congo Red: An acid dye used in testing for hydrochloric acid in gastric contents. It is also used histologically to test for AMYLOIDOSIS.Genome-Wide Association Study: 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.Enzyme-Linked Immunosorbent Assay: 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.Endopeptidases: A subclass of PEPTIDE HYDROLASES that catalyze the internal cleavage of PEPTIDES or PROTEINS.Blotting, Western: 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.Follow-Up Studies: 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.Hypokinesia: 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.Sensitivity and Specificity: 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)Peptides: 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.Protein Processing, Post-Translational: 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.alpha-Synuclein: A synuclein that is a major component of LEWY BODIES that plays a role in neurodegeneration and neuroprotection.Hydrocephalus, Normal Pressure: 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)Neuroprotective Agents: 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.Analysis of Variance: A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.Cell Line: Established cell cultures that have the potential to propagate indefinitely.Blood-Brain Barrier: 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.Early Diagnosis: 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.Osteopathic Physicians: 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.Huntington Disease: 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)Cerebrovascular Circulation: The circulation of blood through the BLOOD VESSELS of the BRAIN.Ethylene Glycols: 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.Protein PrecursorsProtein Isoforms: Different forms of a protein that may be produced from different GENES, or from the same gene by ALTERNATIVE SPLICING.Neprilysin: 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.Extrapyramidal Tracts: 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.Heterozygote: An individual having different alleles at one or more loci regarding a specific character.Cognitive Reserve: Capacity that enables an individual to cope with and/or recover from the impact of a neural injury or a psychotic episode.Immunotherapy, Active: 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.Neurites: 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.Cerebrovascular Disorders: 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.Brief Psychiatric Rating Scale: 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)Acetylcholinesterase: 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 3.1.1.7.Mice, Inbred C57BLHEK293 Cells: A cell line generated from human embryonic kidney cells that were transformed with human adenovirus type 5.Encephalitis: 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)

*Brain morphometry

... in particular neurodegenerative diseases (like Alzheimer) or psychotic disorders (like schizophrenia). MR imaging is rarely ... Brain diseases are the field to which brain morphometry is most often applied, and the volume of the literature on this is vast ... disease and evolution. Since autopsy-like dissection is generally impossible on living brains, brain morphometry starts with ...

*Binswanger's disease

There are many diseases similar to Binswanger's disease including CADASIL syndrome and Alzheimer's disease, which makes this ... Alzheimer renamed this disease Binswanger's disease. In the late 19th century vascular dementia was heavily studied, however by ... "Capillary beds are decreased in Alzheimer's disease, but not in Binswanger's disease". Neuroscience Letters. 417 (2): 128-131. ... It was described by Otto Binswanger in 1894, and Alois Alzheimer first used the phrase "Binswanger's disease" in 1902. However ...

*Amyloid beta

Maslow K (Mar 2008). "2008 Alzheimer's disease facts and figures". Alzheimer's & Dementia. 4 (2): 110-33. doi:10.1016/j.jalz. ... Citron M (Sep 2004). "Strategies for disease modification in Alzheimer's disease". Nature Reviews. Neuroscience. 5 (9): 677-85 ... "Alzheimer diseases: a model of gene mutations and susceptibility polymorphisms for complex psychiatric diseases". American ... transgenic mouse model of Alzheimer's disease". Neurobiology of Disease. 39 (3): 409-22. doi:10.1016/j.nbd.2010.05.013. PMC ...

*Amyloid precursor protein

Chen X, Stern D, Yan SD (Dec 2006). "Mitochondrial dysfunction and Alzheimer's disease". Current Alzheimer Research. 3 (5): 515 ... Koo EH (Nov 2002). "The beta-amyloid precursor protein (APP) and Alzheimer's disease: does the tail wag the dog?". Traffic. 3 ( ... Maynard CJ, Bush AI, Masters CL, Cappai R, Li QX (Jun 2005). "Metals and amyloid-beta in Alzheimer's disease". International ... Tickler AK, Wade JD, Separovic F (Aug 2005). "The role of Abeta peptides in Alzheimer's disease". Protein and Peptide Letters. ...

*Alzheimer's disease research

... relevance to Alzheimer's disease". Journal of Alzheimer's Disease. 10 (1): 89-109. CS1 maint: Explicit use of et al. (link) CS1 ... may benefit patients with Alzheimer's disease. The study used a mouse model of Alzheimer's disease and an antibody against PD-1 ... therapy with Rember arrests disease progression in mild and moderate Alzheimer's disease over 50 weeks". Alzheimer's & Dementia ... Christensen DD (2007). "Alzheimer's disease: progress in the development of anti-amyloid disease-modifying therapies". CNS ...

*Dysexecutive syndrome

Patients with Alzheimer's disease have been shown to exhibit impairment in executive functioning as well. The effects of DES ... Alzheimer's disease Executive functions Frontal lobe disorder Schizophrenia Halligan, P.W., Kischka, U., & Marshall, J.C. (2004 ... are some of the earliest indicators of Alzheimer's. Studies have also indicated that chronic alcoholism (see Korsakoff's ...

*Postoperative cognitive dysfunction

Delirium and severe worsening of mental function is very likely in those with clinically evident Alzheimer's disease or other ... Animal studies indicate that volatile anaesthestics may augment the pathological processes of Alzheimer's Disease by affecting ... MCI is a transitional zone between normal mental function and evident Alzheimer's disease or other forms of dementia. It is ...

*Alzheimer's disease organizations

Alzheimer Disease International - Website Alzheimer Research Forum Alzheimer's South Africa - Website Alzheimer Europe - ... Website Deutsche Alzheimer Gesellschafte e.V - Website The Alzheimer Society of Ireland - Website Alzheimer Nederland - Website ... Website Alzheimer's Australia - Website Alzheimer Society of Canada - Website Alzheimer Society of Ontario - Website ... List of different Alzheimer's Disease Organizations in different countries around the world ...

*Rush Alzheimer's Disease Center

"Rush Alzheimer's Disease Center". Rush University Medical Center. "Alzheimer's Disease Research Centers". National Institute on ... The Rush Alzheimer's Disease Center is one of 29 Alzheimer's centers in the U.S. designated and funded by the National ... The Rush Alzheimer's Disease Center (RADC) is a research center located in Rush University Medical Center. ... The RADC is a leader in research into the causes and treatment of Alzheimer's disease. One of its earliest research projects ...

*Timeline of Alzheimer's disease

"Alzheimer's Society/Alzheimer Nederland knowledge exchange fellowships". Retrieved 13 August 2016. "Alzheimer's Disease ... Molecular Pathology of Alzheimer's Disease. p. 9. "History Module: Dr. Alois Alzheimer's First Cases". Retrieved 11 August 2016 ... "About Alzheimer's Australia". Retrieved 13 August 2016. "National Alzheimer's Disease Awareness Month". Retrieved 11 August ... "Historique de la maladie Alzheimer". Retrieved 11 August 2016. "Treatments for Alzheimer's disease". Retrieved 11 August 2016. ...

*Biochemistry of Alzheimer's disease

... a genetic risk factor for Alzheimer's disease), as well as in inherited forms of Alzheimer's disease. Given that DCGM occurs ... Alzheimer's disease has been identified as a protein misfolding disease, or proteopathy, due to the accumulation of abnormally ... Imaging studies have shown decreased utilization of glucose in the brains of Alzheimer's disease patients early in the disease ... Castellni RJ, Perry G, Smith MA (2004). "Prion disease and Alzheimer's disease: pathogenic overlap". Acta Neurobiol Exp (Wars ...

*Alzheimer's Disease Neuroimaging Initiative

Rafii, Michael S. (2014-01-01). "Preclinical Alzheimer's disease therapeutics". Journal of Alzheimer's disease: JAD. 42 Suppl 4 ... "Alzheimer Disease Biomarkers as Outcome Measures for Clinical Trials in MCI". Alzheimer Disease and Associated Disorders. 29 (2 ... Alzheimer's Disease Neuroimaging Initiative (2015-07-01). "The Alzheimer's Disease Neuroimaging Initiative phase 2: Increasing ... Alzheimer's Disease Neuroimaging Initiative (2015-01-01). "Empowering imaging biomarkers of Alzheimer's disease". Neurobiology ...

*Alzheimer's Disease Cooperative Study

The Alzheimer's Disease Cooperative Study (ADCS) was founded at University of California San Diego in 1991 and coordinates ... "Paul Aisen, MD, Joins Faculty of UCSD and is Appointed New Director of the Alzheimer's Disease Cooperative Study". Journal of ... Fikes, Bradley J. (2 August 2015). "Next steps for scientist in eye of UCSD-USC Alzheimer's spat". San Diego Tribune. Wang, ... Potter, Matt (January 11, 2016). "Deal gives UCSD "read only" rights to Alzheimer's data". San Diego Reader. "Case 3:15-cv- ...

*Journal of Alzheimer's Disease

"Journal of Alzheimer's Disease". 2014 Journal Citation Reports. Web of Science (Science ed.). Thomson Reuters. 2015. Official ... Neuroscience portal The Journal of Alzheimer's Disease is a peer-reviewed medical journal published by IOS Press covering the ... The awardee is presented the Alzheimer Medal, a 3" bronze medal with the likeness of Alois Alzheimer. This yearly award is ... and psychology of Alzheimer's disease. The journal publishes research reports, reviews, short communications, hypotheses, ...

*Depression of Alzheimer disease

Depression is one of the most common psychiatric symptoms in Alzheimer's disease, occurring at all stages of the disease, but ... The symptoms of dAD can arise at any point during the course of Alzheimer's disease, often at a stage quite late in cognitive ... A clinical trial testing sertraline (Zoloft) for depression of Alzheimer disease, launched by the NIMH in 2004, is due to be ... Therefore, dAD often goes unrecognized within the spectrum of symptoms of Alzheimer's disease. In general, people who have dAD ...

*Alzheimer Disease and Associated Disorders

... is a quarterly peer-reviewed medical journal publishing original research findings ... and new approaches to diagnosis and treatment for Alzheimer's disease and related disorders. Official website. ...

*Cell-Cycle Hypothesis of Alzheimer's Disease

... the cell-cycle hypothesis of Alzheimer's disease considers AD as a disease of deregulation of the cell cycle in neurons. The ... Oxidative imbalance in Alzheimer's disease.*J Cell Biochem. 1995 Jun;58(2):160-74. Apoptosis and the cell cycle. Vincent et al ... Alzheimer's Disease (AD) is a neurodegenerative condition characterized by two hallmarks: senile plaques and the ... 1998 Dec;87(4):731-9. The cell division cycle and the pathophysiology of Alzheimer's disease. Nagy et al., 1998. J Cell Biochem ...

*Ion channel hypothesis of Alzheimer's disease

"The amyloid beta ion channel hypothesis of Alzheimer's disease". Neuropsychiatric Disease and Treatment. 3 (5): 597-612. ISSN ... prion diseases, Parkinson's disease, and Huntington's disease. Consistent with Aβ channels, other amyloid channels have also ... The ion channel hypothesis of Alzheimer's disease (AD), also known as the channel hypothesis or the amyloid beta ion channel ... Arispe, N; Rojas, E; Pollard, H B (1993-01-15). "Alzheimer disease amyloid beta protein forms calcium channels in bilayer ...

*American Journal of Alzheimer's Disease & Other Dementias

The American Journal of Alzheimer's Disease & Other Dementias is a peer-reviewed academic journal that publishes papers in the ... The American Journal of Alzheimer's Disease & Other Dementias is abstracted and indexed in, among other databases: SCOPUS, and ... The American Journal of Alzheimer's Disease & Other Dementias is aimed primarily at professionals on the frontline of ... Alzheimer's care, dementia and clinical depression and other specialists who manage patients with dementias and their families ...

*HSD17B10

Beyreuther K, Masters CL (Oct 1997). "Alzheimer's disease. The ins and outs of amyloid-beta". Nature. 389 (6652): 677-8. doi: ... Yang SY, He XY (2001). "Role of type 10 17beta-hydroxysteroid dehydrogenase in the pathogenesis of Alzheimer's disease". ... including 17β-HSD10 deficiency and Alzheimer's disease (AD). Missense and silent mutations in the gene are the cause of ... hydroxyacyl-coenzyme A dehydrogenase is identical to an amyloid beta-peptide-binding protein involved in Alzheimer's disease". ...

*MIND diet

"2017 Alzheimer's Disease Facts and Figures" (PDF). Alzheimer's Association. "Changing the Trajectory of Alzheimer's Disease: ... "MIND diet associated with reduced incidence of Alzheimer's disease". Alzheimer's & Dementia. 11 (9): 1007-1014. doi:10.1016/j. ... The study showed that all the diets can be protective against the development of Alzheimer's disease when they are strictly ... 2016). Association of the MIND diet with cognition and risk of Alzheimer's disease. Curr Opin Lipidol. 27(3):303-4. doi:10.1097 ...

*List of patient-reported quality of life surveys

... disease state, or psychological well-being. Alzheimer's disease. The Quality of Life of Carers of Alzheimer's Disease Patients ... Kidney disease. The Kidney Disease Quality of Life (KD-QOL) Instrument was developed in 1994 by the RAND corporation. It has ... Chronic obstructive pulmonary disease. The Living with Chronic Obstructive Pulmonary Disease questionnaire (LCOPD) has 22 yes ... ACQLI) is a measure which assesses the quality of life of people who care for Alzheimer's disease patients. It was developed in ...

*Huntington's disease

... familial Alzheimer's disease and breast cancer. The European Molecular Genetics Quality Network have published yearly external ... "The Venezuela Huntington's disease project". Hereditary Disease Foundation website. Hereditary Disease Foundation. 2008. ... How far the disease has progressed can be measured using the unified Huntington's disease rating scale, which provides an ... The disease affects men and women equally. Complications such as pneumonia, heart disease, and physical injury from falls ...

*Tetrahydrocannabinol

Alzheimer's disease. A 2011 Cochrane Review found insufficient evidence to conclude whether cannabis products have any utility ... in the treatment of Alzheimer's disease. Tourette syndrome. The available data was determined to be insufficient to allow ... the symptoms of Huntington disease as the available trials were too small to reliably detect any difference Parkinson's disease ... but there was insufficient evidence to determine effectiveness for treating several other neurological diseases. A 2015 review ...

*Cannabis in Delaware

Qualifying conditions include "cancer; Alzheimer's disease; post-traumatic stress disorder; and conditions that cause ...

*Avid Radiopharmaceuticals

Alois Alzheimer in 1906, the only certain way to determine if a person indeed had the disease was to perform an autopsy on the ... In results presented in July 2010 to an international conference on Alzheimer's disease held in Hawaii, the company showed that ... Avid's technique is being used to test the efficacy of Alzheimer's disease treatments being developed by other pharmaceutical ... "Avid Radiopharmaceuticals Initiates First Phase II Trial Of Novel Compound For Imaging Alzheimer's Disease", Medical News Today ...

*Geriatric psychology

"Alzheimer's Disease & Dementia , Alzheimer's Association". www.alz.org. Retrieved 2016-12-12. "Vascular Dementia , Signs, ... a geriatric psychologist's role regarding Alzheimer's disease is the assessment, treatment, and research of the disease. ... Alzheimer's disease is the most common type of dementia, accounting for 60-80 percent of dementia cases. Similar to dementia, ... Parkinson's disease is a movement disorder that has symptoms like tremors, slowing down, stiffness, and impaired balance. A ...
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.
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 ...
PMID: Ayu. 2012 Oct ;33(4):499-504. PMID: 23723666. Abstract Title: Effects of turmeric on Alzheimers disease with behavioral and psychological symptoms of dementia. Abstract: We describe here three patients with the Alzheimers Disease (AD) whose behavioral symptoms were improved remarkably as a result of the turmeric treatment, which is the traditional Indian medicine. Their cognitive decline and Behavioral and Psychological Symptoms of Dementia (BPSD) were very severe. All three patients exhibited irritability, agitation, anxiety, and apathy, two patients suffer from urinary incontinence and wonderings. They were prescribed turmeric powder capsules and started recovering from these symptoms without any adverse reaction in the clinical symptom and laboratory data. After 12 weeks of the treatment, total score of the Neuro-Psychiatric Inventory-brief questionnaire decreased significantly in both acuity of symptoms and burden of caregivers. In one case, the Mini-Mental State Examination (MMSE) ...
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 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.. ...
Volunteer with ALZHEIMERS DISEASE AND RELATED DISORDERS ASSOCIATION. Find ALZHEIMERS DISEASE AND RELATED DISORDERS ASSOCIATION volunteering opportunities at VolunteerMatch!
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 ...
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 ...
Objectives To investigate the rate of platelet thromboxane (TX) biosynthesis and its determinants in Alzheimers disease. Methods and results A cross-sectional comparison of urinary 11-dehydro-TXB2 and 8-iso-prostaglandin (PG)F2α (markers of in vivo platelet activation and lipid peroxidation, respectively), plasma Vitamin E, C-reactive protein (CRP), tumor necrosis factor (TNF)-α and interleukin (IL)-6, was carried-out in 44 Alzheimer patients and 44 matched controls. To investigate the cyclooxygenase (COX)-isoform involved in TXA2 biosynthesis, nine Alzheimer patients were treated with low-dose aspirin (100 mg/d) or rofecoxib (25 mg/d) for 4 days. Urinary 11-dehydro-TXB2 and 8-iso-PGF2α were significantly higher in Alzheimer patients than in controls (Median: 1983.5 versus 517.5 pg/mg creatinine and 938.5 versus 304.0 pg/mg creatinine, p , 0.0001, respectively), with a significant correlation between the two metabolites (ρ = 0.75, p , 0.0001). An inverse correlation was observed between ...
A recent scan of single nucleotide polymorphisms (SNPs) in the region 40-107 Mb on chromosome 10q in a large Japanese case-control cohort identified six SNPs in or near the dynamin-binding protein gene (DNMBP) that were associated with late onset Alzheimers disease (LOAD) in individuals lacking the APOE ε4 allele [Kuwano et al. (2006); Hum Mol Genet 15:2170-2182]. We genotyped these six SNPs in 1,212 unrelated Caucasian patients of UK origin with LOAD and 1,389 ethnically, gender and age matched control subjects. We did not observe a statistically significant association with the risk of LOAD for any of the six SNPs in the sample as a whole. When stratifying the sample by APOE one SNP (intergenic SNP rs11190302) was associated with LOAD in individuals lacking the ε4 allele (genotypic P = 0.027, allelic P = 0.066). However this association was in the opposite direction to that detected in the Japanese population. It remains to be determined whether DNMBP is associated with LOAD. © 2008 ...
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 ...
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 ...
Clinical Question: Are cholinesterase inhibitors safe and effective in patients with Alzheimers dementia?. Setting: Various (meta-analysis). Study Design: Meta-analysis (randomized controlled trials). Synopsis: A previous meta-analysis of functional and behavior outcomes found little benefit with use of cholinesterase inhibitors in patients with Alzheimers dementia (JAMA 2003;289:210-6). In the current study, the primary outcome was "global response," which was defined as minimal improvement or better as evaluated by clinicians (Clinical Global Impression of Change scale) or clinicians and caregivers (Clinicians Interview-Based Impression of Change Plus Caregiver Input scale). A secondary outcome was "cognitive response," defined as an improvement of 4 points or more on the Alzheimers Disease Assessment Scale-Cognitive subscale.. The authors identified 40 studies but excluded 24 because of methodologic problems, leaving 16 studies with more than 7,800 patients for the final analysis. The ...
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 ...
The uridine nucleotide-activated P2Y2, P2Y4 and P2Y6 receptors are widely expressed in the brain and are involved in many CNS processes, including those which malfunction in Alzheimers disease (AD). However, the status of these receptors in the AD neocortex, as well as their putative roles in the pathogenesis of neuritic plaques and neurofibrillary tangles, remain unclear. In this study, we used immunoblotting to measure P2Y2, P2Y4 and P2Y6 receptors in two regions of the postmortem neocortex of neuropathologically assessed AD patients and aged controls. P2Y2 immunoreactivity was found to be selectively reduced in the AD parietal cortex, while P2Y4 and P2Y6 levels were unchanged. In contrast, all three receptors were preserved in the occipital cortex, which is known to be minimally affected by AD neuropathology. Furthermore, reductions in parietal P2Y2 immunoreactivity correlated both with neuropathologic scores and markers of synapse loss. These results provide a basis for considering P2Y2 receptor
Most people with Alzheimers disease have the late-onset form of the disease, in which symptoms become apparent in their mid-60s.The apolipoprotein E (APOE) gene is involved in late-onset Alzheimers. This gene has several forms. One of them, APOE ε4, increases a persons risk of developing the disease and is also associated with an earlier age of disease onset. However, carrying the APOE ε4 form of the gene does not mean that a person will definitely develop Alzheimers disease, and people with no APOE ε4 may also develop the disease.. Also, scientists have identified a number of regions of interest in the genome (an organisms complete set of DNA) that may increase a persons risk for late-onset Alzheimers to varying degrees.. Early-onset Alzheimers disease occurs in people age 30 to 60 and represents less than 5 percent of all people with Alzheimers. Most cases are caused by an inherited change in one of three genes, resulting in a type known as early-onset familial Alzheimers disease, ...
The Pentacam HR Scheimpflug imaging was performed on 10 eyes from 10 Alzheimers disease patients and 10 eyes of 10 age and sex matched control patients (Figure). The average age of Alzheimers disease patients was 72.3±9.9 years and that of control patients was 68.3±6.78 years. The average and maximum densities of the supranuclear lens region were consistently higher in Alzheimers disease patients (12.28±1.25 and 24.72±6.01, respectively), when compared to age and sex matched controls (11.82±1.67 and 22.40±4.3). However, there was no statistically significant difference in these variables between the two groups (p=0.33 and p=0.50).. ...
The progression and symptoms of early-onset Alzheimers Disease, typically identified in patients in their 40s or 50s, can vary dramatically depending on the individual. According to the Alzheimers Association,
The study involved 20 subjects with Alzheimers disease or mild cognitive impairment who, on separate days, were given either emulsified MCTs or a placebo. The researchers observed a significant increase in blood plasma levels of the ketone body beta-hydroxylutyrate (beta-OHB) after only 90 minutes of treatment, and depending on the apolipoprotein E genotype of the subject tested, beta-OHB levels either continued to rise or held constant between the 90 and 120 minute blood draws in the treatment condition. Remarkably, cognitive testing revealed that this brief MCT treatment facilitated improved performance on the Alzheimers Disease Assessment Scale-Cognitive Subscale (ADAS-cog) in 4 subjects within the study group. Moreover, "higher ketone values were associated with greater improvement in paragraph recall with MCT treatment relative to placebo across all subjects (P=0.02)."[i ...
On October 4, the Alzheimer Society of B.C., Brain Canada, Genome British Columbia, the Michael Smith Foundation for Health Research and the Pacific Alzheimer Research Foundation will have an in-depth discussion of how research is moving towards a cure for Alzheimers disease and other dementias. An expert panel will break down the current state of dementia research, including the crucial role played by individuals and families living with the disease. Afterwards, a Q&A session will open the floor for public discussion.. If you or someone in your life is living with the disease, or if youre interested in how B.C. researchers are confronting it, dont miss out. Registration is free, but spaces are limited.. Event details: ...
The CLU gene is located on p21-p12 of human chromosome 8, with CLU as its encoded product, which has various physiological functions, including participating in lipid metabolism (28), oxidative stress reaction (29), and cell cycle regulation (30). CLU is highly expressed in cerebrospinal fluid and amyloid plaques in brain tissues, and is involved in the pathogenesis of AD (4,5,31). Yerbury et al (32) demonstrated that the deposition of CLU in senile plaques and neurofibrillary tangles of AD. Howlett et al (33) further reported a correlation between CLU and senile plaque Aβ40 in the brain cortex of patients with AD. Martin-Rehrmann et al (34) demonstrated the presence of dysfunctional neurons with phosphorylated tau protein surrounding the senile plaques in 71% of CLU-positive patients with AD. Furthermore, they also showed that the tau and phosphorylated tau protein were significantly increased in the rat hippocampus, following the injection of a CLU-rich solution (34). It was suggested that ...
The new potential treatment offers a different approach from the traditional tactic of targeting the amyloid plaques and tangles that develop in the brains of Alzheimers patients. Until recently, most researchers believed these plaques and tangles caused the cognitive decline. But the failure of this hypothesis to lead to an effective treatment for Alzheimers disease has caused some scientists to theorize that, though the plaques and tangles are always associated with the disease, they may not be the main cause of the dementia, nor the best target for treating it ...
Objective: To investigate the particular pathology of the Arctic APP (APParc) early-onset familial Alzheimer disease (eoFAD) mutation for the first time in vivo with PET in comparison with other eoFAD mutations and sporadic Alzheimer disease (sAD).. Methods: We examined 2 APParc mutation carriers together with 5 noncarrier siblings cross-sectionally with C-11-labeled Pittsburgh compound B (PiB) and F-18-fluorodeoxyglucose (FDG) PET, as well as MRI, CSF biomarkers, and neuropsychological tests. Likewise, we examined 7 patients with sAD, 1 carrier of a presenilin 1 (PSEN1) mutation, 1 carrier of the Swedish APP (APPswe) mutation, and 7 healthy controls (HCs).. Results: Cortical PiB retention was very low in the APParc mutation carriers while cerebral glucose metabolism and CSF levels of A beta(1-42), total and phosphorylated tau were clearly pathologic. This was in contrast to the PSEN1 and APPswe mutation carriers revealing high PiB retention in the cortex and the striatum in combination with ...
Alzheimers disease is hypothesized to be caused by an imbalance between β-amyloid (Aβ) production and clearance leading to Aβ accumulation in the central nervous system (CNS). Aβ production and clearance are key targets in the development of disease-modifying therapeutic agents for Alzheimers disease. However, there has not been direct evidence of altered Aβ production or clearance in Alzheimers disease. Using metabolic labeling, we measured Aβ42 and Aβ40 production and clearance rates in the CNS of participants with Alzheimers disease and cognitively normal controls. Clearance rates for both Aβ42 and Aβ40 were impaired in Alzheimers disease compared to controls. On average, there were no differences in Aβ40 or Aβ42 production rates. Thus, the common late-onset form of Alzheimers disease is characterized by an overall impairment in Aβ clearance.. ...
Dr. Lawrence Honigs principal medical and scientific interests are in aging and neurodegenerative diseases of the brain. These latter include Alzheimers disease, Lewy Body dementia, vascular cognitive impairment, and Creutzfeldt-Jakob disease, and also include the frontotemporal degeneration disease family including corticobasal degeneration, ALS-dementia, and progressive aphasia. His laboratory efforts are concentrated on molecular processes that occur in aging and degenerative brain diseases, including changes in chromosomal telomeres, and changes involved in protein processing and in the losses of nerve cells and their connections, the synapses. His research involves analysis of changes in human blood, fluid, and tissues, as well as the use of model systems including mice and cell culture. In addition to his laboratory investigations, he carries out clinical research on diagnosis, imaging, and drug treatment trials of patients with Alzheimers disease and other degenerative brain ...
The statistics on Alzheimers disease are daunting. More than five million Americans are living with the disease and by 2050 this number could be as high as 16 million. Alzheimers is the sixth leading cause of death in the United States, but the only disease among the top ten killers that cannot be prevented, slowed or cured. In fact, Alzheimers disease drug candidates have one of the highest failure rates of any disease area. The resulting human and economic tolls are significant: in 2017, Alzheimers and other dementias will cost the nation $259 billion. Yet, there is a potential, flickering light at the end of the tunnel. Dr. Li-Huei Tsai, Picower Professor of Neuroscience at MIT, and her team of researchers have discovered that LED lights, flickering at a specific frequency, substantially reduce the beta amyloid plaques seen in Alzheimers disease, in the visual cortex of mice. Their work was published in the journal Nature in December 2016. If this finding bears out in humans, it is a ...
Alzheimers Association. 2015 Alzheimers Disease Facts and Figures. Washington, DC: Alzheimers Association. www.alz.org/facts/downloads/facts_figures_2015.pdf. Accessed September 15, 2015. Galvin JE, Sadowsky CH; NINCDS-ADRDA. Practical guidelines for the recognition and diagnosis of dementia. J Am Board Fam Med. 2012;25(3):367-382. PMID: 22570400 www.ncbi.nlm.nih.gov/pubmed/22570400. Knopman DS. Alzheimer disease and other dementias. In: Goldman L, Schafer AI, eds. Goldmans Cecil Medicine. 25th ed. Philadelphia, PA: Elsevier Saunders; 2016:chap 402. Mitchell SL. CLINICAL PRACTICE. Advanced dementia. N Engl J Med. 2015;372(26):2533-2540. PMID: 26107053 www.ncbi.nlm.nih.gov/pubmed/26107053. Peterson R, Graff-Radford J. Alzheimer disease and other dementias. In: Daroff RB, Jankovic J, Mazziotta JC, Pomeroy SL, eds. Bradleys Neurology in Clinical Practice. Philadelphia, PA: Elsevier; 2016:chap 95. ...
Its often stated as fact that Alzheimers disease is the result of a buildup of beta-amyloid plaques in your brain. Such plaques may increase in your brain as you age, but tend to be far more abundant in people with Alzheimers disease.. Some people have a genetic mutation known to increase the production of beta-amyloid, but in most people the cause behind such buildup is unknown.. Provocative new research suggests that beta-amyloid buildup may not be intrinsically abnormal, and instead, may act as a natural antibiotic that protects your brain from infection. Alzheimers disease, then, might be a byproduct of your brains attempts to fight off infections.. Alzheimers Disease as a Byproduct of Infectious Disease. Harvard researchers have suggested that beta-amyloid proteins are antimicrobial peptides (part of your innate immune response) and have a beneficial role to play in your brain.. If viruses or bacteria cross your blood-brain barrier, the beta-amyloid traps the foreign invader and ...
When Patrick Conaboy, M.D., was a teen, he was among the family members who helped take care of his grandmother. "She lived to exactly her 100th birthday, as she always told us she would," Dr. Conaboy said with a chuckle. Grandma Conaboy had her wits about her up until the very end. The same cannot be said for the many Alzheimers patients Dr. Conaboy treats on a daily basis. And, unfortunately, theres only so much he can do for them. Geriatric care is among the primary focuses for Dr. Conaboy, a longtime family practitioner who shares a practice with Dr. Peter Cognetti in the McAuley Building, 802 Jefferson Ave. Hes also the medical director at Lackawanna County Health Care Center and Holy Family Residence, as well as the outpatient medical director for Mercy Hospice. As he looks back on the more than two decades hes been practicing, Dr. Conaboy doesnt see much to get excited about when it comes to the treatment of Alzheimers disease.. "Id like to say there have been great strides, but ...
The impact of Alzheimers disease on caregivers and families is staggering. Fortunately, there are effective strategies for overall management that are covered in this guideline.. The Guidelines for Alzheimers Disease Management were developed through the California Workgroup on Alzheimers Disease Management. These guidelines provide basic recommendations for the ongoing care and management of persons with Alzheimers Disease.. The guidelines are intended for primary care providers including physicians, nurse practitioners, physician assistants, social workers and other practitioners who provide care to persons with Alzheimers and their families. It is assumed that a proper diagnosis of Alzheimers Disease has been made before these recommendations are followed.. Californias Caregiver Resource Centers and the Alzheimers Association are the two organizations identified for caregiver education and support.. For more information on the guidelines or to order an information packet, please ...
Shriver Report Shows Alzheimers Impact on Women:. Aging Pros Challenges and Solutions. Dr Cheryl Mathieu. The Shriver Report: A Womens Nation Take on Alzheimers was just released. The Report is a collaboration between Maria Shriver and the Alzheimers Association, exposing the epidemics effect on women as caregivers, advocates and people with the disease. Maria is getting people talking about Alzhiemers disease!. Alzheimers is a womens issue. According to the report, women make up two-thirds of the people with Alzheimers in the U.S. and account for 60 percent of the unpaid caregivers for people with Alzheimers. This means that 10 million women either have Alzheimers or are caring for someone with Alzheimers. 40 percent of the caregivers interviewed said they felt like they had no choice in assuming the caregiving role. These numbers continue to grow, daily.. Alzheimers disease is costly. Governments, businesses and families spend $300 billion a year on Alzheimers disease. Yearly, ...
Importance: Late-onset Alzheimer disease (AD) is highly heritable. Genome-wide association studies have identified more than 20 AD risk genes. The precise mechanism through which many of these genes are associated with AD remains unknown. Objective: To investigate the association of the top 20 AD risk variants with brain amyloidosis. Design, Setting, and Participants: This study analyzed the genetic and florbetapir F 18 data from 322 cognitively normal control individuals, 496 individuals with mild cognitive impairment, and 159 individuals with AD dementia who had genome-wide association studies and 18F-florbetapir positron emission tomographic data from the Alzheimers Disease Neuroimaging Initiative (ADNI), a prospective, observational, multisite tertiary center clinical and biomarker study ...
The Shriver Report: A Womens Nation Take on Alzheimers was just released. The Report is a collaboration between Maria Shriver and the Alzheimers Association, exposing the epidemics effect on women as caregivers, advocates and people with the disease. Maria is getting people talking about Alzhiemers disease!. Alzheimers is a womens issue. According to the report, women make up two-thirds of the people with Alzheimers in the U.S. and account for 60 percent of the unpaid caregivers for people with Alzheimers. This means that 10 million women either have Alzheimers or are caring for someone with Alzheimers. 40 percent of the caregivers interviewed said they felt like they had no choice in assuming the caregiving role. These numbers continue to grow, daily.. Alzheimers disease is costly. Governments, businesses and families spend $300 billion a year on Alzheimers disease. Yearly, it costs about $56,000 to care for someone with Alzheimers, which is typically paid for by families. ...
Our data comparing late onset, necropsy confirmed AD cases to non-demented controls (matched for age and sex) are consistent with those of Lambert et al,3 in that the A allele of the 3′UTR polymorphism was associated with a reduction in the risk of AD. The rare A allele, found in 8% of controls, appears to confer a protective effect. The magnitude of this effect (OR=0.59 for A allele) is similar to that described in the combined samples of Lambert et al 3 (OR=0.60). It is also reassuring that the allele and genotype frequencies in our cases and controls were similar to those reported by Lambert et al.3 For instance, the A allele was found in 4% of the pooled cases and 7% of the pooled controls described previously,3 and in 5% of our cases and 8% of our controls. We observed no significant differences between the genotype frequencies in the cases and controls. This is probably because there are twice as many alleles as genotypes, which therefore results in a greater power to detect an effect. ...
If you have experience caring for someone with Alzheimers or dementia, you know that confusion can surface in so many ways. We help Alzheimers patients in NYC
Alzheimers disease (AD) is the most common age-related dementia, with the number of affected individuals expected to exceed 100 million worldwide by 2050. In Australia, Alzheimers disease is the third leading cause of death behind heart disease and cancer. Despite the significance of this disease there are currently no disease modifying drugs to treat Alzheimers disease.. One of the pathological hallmarks of Alzheimers disease is the cerebral deposition of plaques composed of Amyloid-beta (Aß) peptide. Aß is produced by sequential proteolytic cleavage of the ubiquitously expressed integral-membrane protein, amyloid ß-protein precursor. The Aß released typically ranges from 38 to 43 amino acids in length due to imprecise cleavage. Peptides Aß1-40 and Aß1-42 are two of the most common forms and have received the majority of research attention. Clearance of Aß is slowed in cerebrospinal fluid from Alzheimers disease patients, which likely contributes to its pathological deposition. The ...
One of the crucial challenges for the future of therapeutic approaches to Alzheimers disease (AD) is to target the main pathological processes responsible for disability and dependency. However, a progressive cognitive impairment occurring after the age of 70, the main population affected by dementia, is often related to mixed lesions of neurodegenerative and vascular origins. Whereas young patients are mostly affected by pure lesions, ageing favours the occurrence of co-lesions of AD, cerebrovascular disease (CVD) and Lewy body dementia (LBD). Most of clinical studies report on functional and clinical disabilities in patients with presumed pure pathologies. But, the weight of co-morbid processes involved in the transition from an independent functional status to disability in the elderly with co-lesions still remains to be elucidated. Neuropathological examination often performed at late stages cannot answer this question at mild or moderate stages of cognitive disorders. Brain MRI, Single Photon
http://people.csail.mit.edu/seneff/alzheimers_statins.html. "Evidence that Infection is Associated with Alzheimers. There is substantial evidence that Alzheimers is related to an increased likelihood of infective agents appearing in the brain. Some researchers believe that infective agents are the principle cause of Alzheimers. There are a number of bacteria that reside in the human digestive system and can co-exist with our own cells without any harm. However, H. pylori, one that is quite common, has been recently shown to be responsible for stomach ulcers. It has been suspected that H. Pylori might be implicated in Alzheimers, and, indeed, a recent study showed that Alzheimers patients had a significantly higher concentration of an antibody against H. Pylori in both their cerebrospinal fluid and their blood than non-Alzheimers controls [26]. H. pylori was detected in 88% of the Alzheimers patients but only 47% of the controls. In an effort to treat the Alzheimers patients, the ...
Immunotherapy with the antibody bapineuzumab in patients with mild to moderate Alzheimer disease resulted in decreases in a cerebrospinal fluid biomarker, which may indicate downstream effects on the degenerative process, according to a report published Online First by Archives of Neurology, a JAMA Network publication.. Alzheimer disease (AD) is a progressive neurodegenerative disease characterized by, among other things, deposits of extracellular β-amyloid (Î β) plaques and intraneuronal neurofibrillary tangles with accompanying decreases in cerebrospinal fluid (CSF) Î β and increases in CSF tau proteins. Bapineuzumab is an anti-Î β monoclonal antibody, and immunotherapy with antibodies against Î β is one of the major disease-modifying therapeutic approaches being evaluated for AD, the authors write in their study background.. Kaj Blennow, M.D., Ph.D., of the University of Gothenburg, Sweden, and colleagues conducted a combined analysis of two double-blind, placebo-controlled trials ...
Researchers studying peptides using the Gordon supercomputer at the San Diego Supercomputer Center (SDSC) at the University of California, San Diego (UCSD) have found new ways to elucidate the creation of the toxic oligomers associated with Alzheimers disease. Igor Tsigelny, a research scientist with SDSC, the UCSD Moores Cancer Center, and the Department of Neurosciences, focused on the small peptide called amyloid-beta, which pairs up with itself to form dimers and oligomers. The scientists surveyed all the possible ways to look at the dynamics of conformational changes of these peptides and the possibility that they might organize into the oligomers theorized to be responsible for the degenerative brain disease. In the February 14 issue of the Journal of Alzheimers Disease, the researchers suggest their results may generate new targets for drug development. "Our research has identified amino acids for point mutations that either enhanced or suppressed the formation and toxicity of oligomer ...
More than 50% of family members who care for Alzheimers patients at home reported that they acted abusively, according to a recent British study.
According to the revised criteria several patients currently diagnosed with very mild or mild Alzheimer disease dementia could be reclassified as having mild cognitive impairment (MCI).
The use of disease-modifying treatments (DMTs) in MS is one of the most rapidly evolving therapeutic areas in neurology. As new and arguably more effective treatments have become available, decision-making in regard to MS DMTs has become much more complex for both neurologists and people with MS. This course will review the mechanisms of action and the risk-benefit ratios of the DMTs and delve into different treatment paradigms, risk mitigation strategies, sequencing considerations, and shared decision making. This program complements Multiple Sclerosis Therapy: Disease-modifying Treatment I, but covers independent topics ...
The use of disease-modifying treatments (DMTs) in MS is one of the most rapidly evolving therapeutic areas in neurology. As new and arguably more effective treatments have become available, decision-making in regard to MS DMTs has become much more complex for both neurologists and people with MS. This course will review the mechanisms of action and the risk-benefit ratios of the DMTs and delve into different treatment paradigms, risk mitigation strategies, sequencing considerations, and shared decision-making. This program complements Multiple Sclerosis Therapy: Disease-modifying Treatment II, but covers independent topics ...
Although the causes of Alzheimers disease are still unknown, it is clear that the disease commences with progressive amyloid deposition in the brains of affected persons between ten and fifteen years before the emergence of initial clinical symptoms such as memory loss. Researchers have now been able to show that Aducanumab, a human monoclonal antibody, selectively binds brain amyloid plaques, thus enabling microglial cells to remove the plaques. A one-year treatment with the antibody, as part of a phase Ib study, resulted in almost complete clearance of the brain amyloid plaques in the study group patients. The results, which were realized by researchers at UZH together with the biotech company Biogen and the UZH spin-off Neurimmune, have been published in the renowned science journal |em|Nature|/em|.
Strong evidence of linkage to late-onset Alzheimer disease (LOAD) has been observed on chromosome 10, which implicates a wide region and at least one disease-susceptibility locus. Although significant associations with several biological candidate genes on chromosome 10 have been reported, these findings have not been consistently replicated, and they remain controversial. We performed a chromosome 10-specific association study with 1,412 gene-based single-nucleotide polymorphisms (SNPs), to identify susceptibility genes for developing LOAD. The scan included SNPs in 677 of 1,270 known or predicted genes; each gene contained one or more markers, about half (48%) of which represented putative functional mutations. In general, the initial testing was performed in a white case-control sample from the St. Louis area, with 419 LOAD cases and 377 age-matched controls. Markers that showed significant association in the exploratory analysis were followed up in several other white case-control sample sets to
The preclinical phase of Alzheimers disease is a future target for treatment, but additional research is essential to understand the relationship between β-amyloid burden and cognition during this time. We investigated this relationship using a large sample of apparently healthy older adults (N = 177), which also enabled examination of whether the relationship differed according to age, gender, years of education, apolipoprotein E status, and the presence of subjective memory complaints. In addition to episodic memory, a range of cognitive measures (global cognition, semantic memory, visuospatial performance, and executive function) were examined. Participants were aged over 60 years with no objective cognitive impairment and came from the imaging arm of the Australian Imaging, Biomarkers, and Lifestyle (AIBL) study of ageing. 11C-PiB PET was used to measure β-amyloid burden and a PiB cut-off level of 1.5 was used to separate participants with low PiB retention from those with high PiB retention.
Disease Markers is a peer-reviewed, Open Access journal that publishes original research articles, review articles, and clinical studies related to the identification of disease markers, the elucidation of their role and mechanism, as well as their application in the prognosis, diagnosis and treatment of diseases.
The study compared 24 gray and white matter samples from patients with the disease - using Consortium to Establish a Registry for Alzheimers disease criteria - with 18 samples from people who had shown no evidence of cognitive decline. While LPS and K99 were found in both groups, the prevalence was much higher in the Alzheimers patients. K99 was found in nine of 13 Alzheimers gray-matter samples compared to one of 10 controls by Western blot analysis. Increased K99 levels were also found in Alzheimers disease white matter samples. The story was similar with LPS, which was found in all six samples (three gray and three white matter) but not in the controls by Western blot analysis.. "Finding bacterial molecules in the brain was a surprise, and finding more in the Alzheimers brains was a great surprise," said Frank Sharp, professor of neurology and senior author on the paper. "People have noted infectious agents in brains. These are the first bacterial molecules that are consistently found in ...
High levels of the protein beta-amyloid in the brain that is associated with Alzheimers disease may affect brain performance even in healthy adults, according to a study published in the Feb. 1, 2012, online issue of Neurology, the medical journal of the American Academy of Neurology.
The design of the study by Tang and colleagues included collection of information about ERT use before the onset of Alzheimer disease, diagnosis of Alzheimer disease without knowledge of past ERT use, and adjustment of the results for many of the risk factors for Alzheimer disease. Thus, the association between ERT use and Alzheimer disease is valid and can be generalized to most elderly women. The validity is further strengthened by a significant dose-response relation: the longer women used ERT, the lower the risk for developing Alzheimer disease. The authors cite earlier studies that link estrogen with the preservation of cholinergic neurons, increased secretase metabolism of the amyloid precursor protein, and interaction with apolipoprotein E-all of which are factors that make a causal association between ERT and the risk for developing Alzheimer disease biologically plausible. As the authors point out, ERT use may also be a marker for behavioral and medical factors that were not controlled ...
Alzheimer Dementia Health: 20 assigned downloads, like Amyotrophic Lateral Sclerosis - , MD Miller, Robert G., Dr. from ebook-reader
Early-onset Alzheimers disease, also known as younger-onset affects people younger than 65, many people with this diagnosis are in their 40s and 50s, they have families and careers when Alzheimers disease strikes. In the United State it is estimated that approximately 200,000 people have early onset Alzheimers.. Getting a diagnosis for this dementia presents serious problems for people under 65. Health care providers generally dont look for the disease in younger patients and it is not uncommon for doctors to say that the symptoms may be related to stress menopause or depression. It can therefore be months or years before the right diagnosis is made and proper treatment can begin.. Although Early-onset Alzheimers disease (EOD) currently has no cure doctors have had some success in helping people maintain function, control behavior and slow the progression of the disease, in addition researchers are learning new things about Alzheimers disease every day.. The medical community does not ...
Neurodegeneration is characterized by dysfunction and death of cells in the nervous system. This results in impaired motor function and progressive dementia. Neurodegenerative diseases include prion disease, Parkinsons disease, Huntingtons disease, Amyotrophic Lateral Sclerosis (Lou Gehrigs disease), and various types of dementia, of which Alzheimers disease is the most common. Intense research focus on Alzheimers disease has identified 2 main pathways leading to characteristic protein deposits in the brain. These are pathologic breakdown of amyloid precursor protein leading to the formation of extracellular amyloid plaques, and hyperphosphorylation of the microtubule associated protein Tau, causing intracellular neurofibrillary tangles. Several genes have confirmed links to Alzheimers disease, and many genotyping and gene expression studies currently in progress aim to elucidate the causes, develop biomarkers for diagnosis, and identify potential drug targets ...
Neurodegeneration is characterized by dysfunction and death of cells in the nervous system. This results in impaired motor function and progressive dementia. Neurodegenerative diseases include prion disease, Parkinsons disease, Huntingtons disease, Amyotrophic Lateral Sclerosis (Lou Gehrigs disease), and various types of dementia, of which Alzheimers disease is the most common. Intense research focus on Alzheimers disease has identified 2 main pathways leading to characteristic protein deposits in the brain. These are pathologic breakdown of amyloid precursor protein leading to the formation of extracellular amyloid plaques, and hyperphosphorylation of the microtubule associated protein Tau, causing intracellular neurofibrillary tangles. Several genes have confirmed links to Alzheimers disease, and many genotyping and gene expression studies currently in progress aim to elucidate the causes, develop biomarkers for diagnosis, and identify potential drug targets ...
COLUMBIA, Mo. -- Alzheimers is a progressive brain disease that affects older adults, slowly destroys their memories and may cause dementia. According to estimates from the National Institutes of Health (NIH), the disease may affect as many as 5.1 million Americans. Now, with the help of a $1.5 million grant from the NIH, University of Missouri researcher James Lee will continue to look for clues into the causes of Alzheimers.. "Alzheimers is an extremely complex disease," said Lee, an associate professor of bioengineering in the MU College of Engineering. "Our research team focuses on a protein, amyloid-beta peptide, which is present at toxic levels in the brains of Alzheimers patients. We hope to find links between the peptide and the inevitable damage to blood capillaries in the brain.". In the brains of Alzheimers patients, amyloid-beta peptide (A-beta) adversely interacts with astrocytes, or star-shaped cells that provide structural and metabolic support to neurons and control ...
The basal forebrain degenerates in Alzheimers disease (AD) and this process is believed to contribute to the cognitive decline observed in AD patients. Impairment in spatial navigation is an early feature of the disease but whether basal forebrain dysfunction in AD is responsible for the impaired navigation skills of AD patients is not known. Our objective was to investigate the relationship between basal forebrain volume and performance in real space as well as computer-based navigation paradigms in an elderly cohort comprising cognitively normal controls, subjects with amnestic mild cognitive impairment and those with AD. We also tested whether basal forebrain volume could predict the participants ability to perform allocentric- vs. egocentric-based navigation tasks. The basal forebrain volume was calculated from 1.5 T MRI scans, and navigation skills were assessed using the human analog of the Morris water maze employing allocentric, egocentric and mixed allo/egocentric real space as well as
On June 17, 2013 the U.S. Department of Health and Human Services (HHS) released the 2013 Alzheimers disease plan update. The initial "National Plan to Address Alzheimers Disease" was released in May 2012 under the 2011 National Alzheimers Project Act (NAPA). President Obama signed the National Alzheimers Project Act to support Alzheimers research and help individuals and families affected by Alzheimers disease. The National Plan to Address Alzheimers disease was developed by experts in Alzheimers disease and aging to discover techniques to prevent and treat Alzheimers disease by 2025, improve care for patients, enhance public awareness, and increase support for caregivers. The 2013 update to the National Plan highlights completed goals over the past year in addition to recommendations for additional action steps. Highlights in the fight against Alzheimers disease this past year include the National Institutes of Health organized the Alzheimers Disease Research Summit in May 2012 to ...
There are 47.5 million people suffering from dementia worldwide, with 7.7 million new cases each year. The most common cause of dementia, Alzheimers disease, makes up 60-70% of cases. (Dementia 2016) Millions of Americans are challenged by Alzheimers disease and other forms of dementia. In 2016, an estimated 5.4 million Americans of various ages are diagnosed with Alzheimers disease, and approximately 5.2 million of those are ages 65 and older. (Alzheimers Disease Facts and Figures 2016). Although Alzheimers is not a new illness, it seems like it has become a household name. The reason for this accelerated trend is that people are living longer now than ever before in history, which is causing the exponential growth of the number of cases of Alzheimers disease. Seniors age 85 and older unfortunately have a 50% chance of developing this disease. In addition, women are more prone to have Alzheimers, partially because they live longer than men. In addition, Alzheimers disease and other ...
Pan Laboratories has presented at the AACC annual meeting Plasma neuron derived exosomal protein biomarkers in the diagnosis of Alzheimers Disease
The PRESENILIN1 and PRESENILIN2 genes encode structurally related proteases essential for ?-secretase activity. Of nearly 200 PRESENILIN mutations causing early onset, familial Alzheimers disease (FAD) only the K115Efx10 mutation of PSEN2 causes truncation of the open reading frame. If translated, the truncated product would resemble a naturally occurring isoform of PSEN2 named PS2V that is induced by hypoxia and found at elevated levels in late onset Alzheimers disease (AD) brains. The function of PS2V is largely unexplored. We show that zebrafish possess a PS2V-like isoform, PS1IV, produced from the fishs PSEN1 rather than PSEN2 orthologous gene. The molecular mechanism controlling formation of PS2V/PS1IV was probably present in the ancient common ancestor of the PSEN1 and PSEN2 genes. Human PS2V and zebrafish PS1IV have highly divergent structures but conserved abilities to stimulate ?-secretase activity and to suppress the unfolded protein response (UPR) under hypoxia. The putative ...
Alzheimers disease is a neurodegenerative disorder typified by the accumulation of a small protein, beta-amyloid, which aggregates and is the primary component of amyloid plaques. Many new therapeutic and diagnostic agents for reducing amyloid plaques have limited efficacy in vivo because of poor transport across the blood-brain barrier. Here we demonstrate that low-intensity focused ultrasound with a microbubble contrast agent may be used to transiently disrupt the blood-brain barrier, allowing non-invasive, localized delivery of imaging fluorophores and immunotherapeutics directly to amyloid plaques. We administered intravenous Trypan blue, an amyloid staining red fluorophore, and anti-amyloid antibodies, concurrently with focused ultrasound therapy in plaque-bearing, transgenic mouse models of Alzheimers disease with amyloid pathology. MRI guidance permitted selective treatment and monitoring of plaque-heavy anatomical regions, such as the hippocampus. Treated brain regions exhibited ...
The purpose of the study is to evaluate safety and the pharmacodynamic effects of BMS-241027 on cerebrospinal fluid (CSF) Tau, connectivity magnetic resonance imaging (MRI), and computerized cognitive tests in mild Alzheimers disease (AD) subjects, following 9 weekly intravenous (IV) infusions of BMS-241027.. ...
Advanced age is a major Alzheimers disease (AD) risk factor; therefore, understanding cellular senescence and its impact on endothelial cells (ECs), neurons, glia, and immune cells is an essential prerequisite for elucidating the pathogenesis of this condition. Brain accumulation of extracellular β-amyloid and intracellular hyperphosphorylated tau are the pathological hallmarks of AD. Both neurons and astrocytes synthesize β-amyloid from amyloid precursor protein (APP), while phagocytic microglia prevent its accumulation by removing it via the triggering receptor expressed on myeloid cells-2 (TREM-2). The amyloid hypothesis postulates that accumulation and deposition of β-amyloid are the primary causes of AD, which promotes tau aggregation into neurofibrillary tangles (NFTs), ultimately triggering neuronal death. Although never universally accepted, the amyloid hypothesis drove AD research for at least two decades. Lately, however, many researchers and clinicians have questioned this model ...
After comparing brain scans to the results of the tests, the research team found that changes in DTI imaging better explained declines in memory than did the traditional MRI. They also discovered that mean diffusivity in the hippocampus, the region of the brain involved in Alzheimers disease, better predicted spatial and verbal memory performance, especially in those at a high-risk age ...
As a caregiver, you shouldnt just keep waiting for the next doctors appointment. Keep track of new practices happening to counter behavioral changes in the patient. Use trusted sites like braintest, mayoclinic or webMD for information regarding common symptoms in the patient. Spending time with the patient will release hormones of calmness in them, making them feel relaxed and loved. You can get a pet, since they are proven to uplift any depressed persons mood.. Being a caregiver you should always know how important your role is in the patients life, and your actions can directly affect the patient in a positive or negative way. There is no big blessing to your loved one than your genuine care. Sit with them and remember the good old days with them, the days that they can remember. Take this responsibility very seriously and keep your head calm in all situations.. ...
The Alzheimers Disease Neuroimaging Initiative (ADNI) was set to begin recruiting this month for its clinical trial (www.alzheimers.org/clintrials/fullrec.asp?PrimaryKey=208) that will study how brain imaging technology can help measure the progression of mild cognitve impairment (MCI) and early Alzheimer disease (AD). 1
Lacey LA, Niecko T, Leibman C, Liu E, Grundman M. J Nutr Health Aging 2013;17:745-50.. Publication date: November 1, 2013. Summary. In patients with Alzheimers disease (AD), dependence has been shown to correlate with impairments in cognition, function and behaviour. In this longitudinal, observational study conducted at 39 sites in the United States and Europe between 2006 and 2009, the authors evaluated the association between dependence (as assessed by the Dependence Scale [DS]), cognitive function (Mini mental State Examination [MMSE] and Alzheimers Disease Assessment Scale−Cognitive Subscale [ADAS-Cog]), functional ability (Disability Assessment for Dementia [DAD]) and neuropsychiatric symptoms (Neuropsychiatric Inventory [NPI]), on the one hand, and resource utilization (Resource Utilization in Dementia Questionnaire), on the other hand.. A total of 196 patients with mild to moderate AD (mean age, 75 years) participated in the study. A complete DS profile was available for 65 patients. ...
The protein amyloid is invariably deposited in the brains of patients with all forms of Alzheimers disease (AD). It is composed of a secreted peptide (Aβ) that can be either 40 or 42 amino acids long (Aβ 1-40 or Aβ 1-42). Aβ 1-42 forms insoluble amyloid fibrils and is deposited early and selectively in the senile plaques that are a pathological hallmark of AD. Our recent studies of plasma Aβ indicate that genetic elevation of Aβ plays a major role in typical late onset AD. This has important therapeutic implications, which we are pursuing using a transgenic mouse model for AD. In addition, we are investigating the possibility that plasma Aβ may be an excellent biomarker of AD and are searching for the genetic determinants that increase Aβ in typical late onset AD.. The amyloid that is invariably deposited in the brains of patients with all forms of Alzheimers disease (AD) is composed of a peptide β amyloid, (Aβ) that is derived from a set of larger proteins collectively referred to ...
The editorial points a finger at three microorganisms: the cold sore-causing Herpes Simplex 1 virus (HSV1), Chlamydia pneumonia bacteria, and various spirochete bacteria such as syphilis, all of which are reportedly present in the brains of many elderly people. For instance, they cite studies that have noted amplification of HSV1 DNA in the brains of immunosuppressed individuals. Furthermore, they write that pathogen hallmarks (such as microbial DNA) tend to co-localize with amyloid plaques in Alzheimers patients. Correlations have been deduced between testing positive for HSV1 infection and developing Alzheimers disease. More recently, Alzheimers has been shown to have a "communicable" feature - features of Alzheimers pathology have been found to be transmissible by inoculation of Alzheimers-afflicted cells to animal models. Similarities between syphilitic dementia (dementia caused by the bacteria that cause syphilis) and Alzheimers disease further underscore a potential connection, and ...
In the article, "Treatment of Alzheimer Disease" (June 15, 2011, page 1403), the first clinical recommendation in the Strength of Recommendation Taxonomy (SORT) table (page 1404) was not as complete or balanced as it should have been. The recommendation, "Acetylcholinesterase inhibitors should be considered first-line therapy for patients with mild to moderate Alzheimer disease," should have mentioned the adverse effects associated with this drug class. The revised recommendation should read: "Acetylcholinesterase inhibitors are modestly effective in patients with mild to moderate Alzheimer disease, although limited by their adverse effects." The article has been corrected online. ...
WASHINGTON, Dec. 23, 2015-- Stephanie Monroe, Executive Director of AfricanAmericansAgainstAlzheimers, released the following statement in support of Hillary Clintons plan to effectively treat, prevent and cure Alzheimers disease by 2025. Read statements from all of UsAgainstAlzheimers networks here. Hillary Clinton took a bold step on behalf of...
Reviews the basic science and clinical knowledge of the role of oxidative stress in the pathology of Alzheimers disease Describes the most current
Bioethics and Alzheimers Disease, a daylong conference on the moral, legal and medical issues related to the debilitating neurological disease, will be held from 8:30 a.m. to 4 p.m. Saturday at
The current paper, written by our professional writers, will research Alzheimers disease, its history, symptoms, breakthroughs in cure, and alternative methods of treatment.
It is believed by many well-known researches that Alzheimers disease, is caused by inflammation. William A. Banks, MD discusses this in two different publ
Methods: The present 15-month double-blind, placebo-controlled trial (NCT01689246) was performed in patients with probable AD, Mini-Mental State Examination (MMSE) score in the range 14-26, Clinical Dementia Rating (CDR) 1-2 and age , 90 years. Patients were randomized 3:3:4 to receive oral LMTM at doses of 150 or 250 mg/day or placebo (containing 8 mg/day, to maintain blinding) respectively. Primary efficacy outcomes were change from baseline on cognitive (Alzheimers Disease Assessment Scale cognitive subscale; ADAS-Cog) and functional (Alzheimers Disease Cooperative Study Activities of Daily Living; ADCS-ADL) scores. Three-monthly assessment included magnetic resonance imaging (MRI) as a disease modifying outcome. Other secondary outcomes included ADCS-CGIC and MMSE ...
This week marks publication of a provocative study by Sparks et al. (Sparks et al., 2005). This study suggests that treatment with atorvastatin reduces the progression of Alzheimer disease (AD) in subjects with mild to moderate forms of the disease. The results show benefits that are statistically significant in multiple categories, including ADAS-COG, GDS, and activities of daily living. In many ways, the results observed by Sparks et al. reproduce results observed in a study reported by Simons et al. three years ago, where they treated patients with mild to moderate Alzheimer disease with simvastatin and observed significant reductions in β amyloid levels and significant decrease in the rate of cognitive loss (Simons et al., 2002). These two small studies both provide evidence that statins can prevent the decline in cognitive function in subjects with mild to moderate Alzheimer disease.. The positive results observed by Sparks and Simons contrast sharply with the negative results reported by ...
Alzheimer Patients can benefit from Ralapure R Alpha Lipoic Acid (R ALA.) Learn how R ALA can exert positive effects in Alzheimer Patients
The differentiation between the Alzheimer and multi-infarct types of dementia may still be equivocal considering clinical criteria, neuropsychological tests, and imaging techniques. Cerebral microangiopathic alterations underlying multi-infarct dementia should allow the characterization of dementia subgroups.. Patients with a diagnosis of multi-infarct dementia (n = 17; mean age, 69.1 +/- 8.5 years) or Alzheimer dementia (n = 24, mean age, 65.8 +/- 9.0 years) according to standard testing criteria, clinical findings, and neuroimaging techniques (computed tomography and magnetic resonance imaging) were investigated prospectively by transcranial Doppler sonography and compared with a normal reference group (n = 64; mean age, 61.0 +/- 11.1 years). Transcranial Doppler sonography allows an indirect evaluation of peripheral flow resistance in the microcirculatory bed by quantifying pulsatility characteristics, as reflected in the effective pulsatility range (time-averaged mean blood flow velocity ...
OBJECTIVE: To assess the transactive response DNA-binding protein 43 (TDP-43) burden in familial forms of Alzheimer disease (FAD) and Down syndrome (DS) to determine whether TDP-43 inclusions are also present. DESIGN: Using standard immunohistochemical techniques, we examined brain tissue samples from 42 subjects with FAD and 14 with DS. RESULTS: We found pathological TDP-43 aggregates in 14.0% of participants (6 of 42 and 2 of 14 participants with FAD and DS, respectively). In both FAD and DS, TDP-43 immunoreactivity did not colocalize with neurofibrillary tangles. Occasionally participants with FAD or DS had TDP-43-positive neuropil threads or dots. Overall, the amygdala was most commonly affected, followed by the hippocampus, with no TDP-43 pathology in neocortical regions. A similar distribution of TDP-43 inclusions is seen in sporadic Alzheimer disease, but it differs from that seen in amyotrophic lateral sclerosis and frontotemporal dementia. CONCLUSIONS: Transactive response DNA-binding ...
The rate of progression in Lewy body dementia (LBD) is hard to predict at the time of diagnosis. New research indicates the presence of a second neurodegenerative disease process, Alzheimers disease (AD), has an impact on ones prognosis.. Researchers from five academic centers pooled clinical and autopsy data from 213 individuals with both clinical and autopsy-confirmed diagnoses of Parkinsons disease dementia or dementia with Lewy bodies (DLB). The subjects were then divided into groups according to the amount of co-existing Alzheimers disease pathology: none (23%), low-level (26%), intermediate level (21%) and high level (30%).. As the level of Alzheimers disease pathology rose, so did the level of Lewy body pathology in the brains cerebrum. This suggests a synergistic effect between the two disease processes. Higher levels of AD pathology were associated with older age at the onset of motor symptoms, dementia and death. Compared to those with no AD pathology, individuals with the ...
Lewy body dementia may not be as well-known as Alzheimers disease, but is the second-most progressive form of dementia after Alzheimers disease.. It causes a progressive decline in mental and physical abilities.. What is Lewy body dementia and what are its symptoms?. Mayo Clinic neuropathologist Dr. Dennis Dickson says, "Lewy body dementia is a prototypical mixed dementia, with features of both Parkinsons disease and Alzheimers disease. This combination of disease processes makes medical management difficult.The four cardinal features are cognitive impairment, visual hallucinations, fluctuations in level of consciousness, and Parkinsonism. Rapid eye movement (REM) sleep behavior disorder (RBD) is another very characteristic feature of many patients.". Mayo Clinic neurologist Dr. Rodolfo Savica says those with Lewy body dementia often show traits of both Alzheimers disease and Parkinsons disease, leading to the concept that it falls between the two disorders. Like Parkinsons disease, Lewy ...
A Written Declaration on Alzheimers disease was launched on 5 October 2015. The Written Declaration was launched by MEPs Dominique Bilde (France), Patricija Šulin (Slovenia), Ivo Vajgl (Slovenia), Luke Ming Flanagan (Ireland), Valentinas Mazuronis (Lithuania), Emilian Pavel (Romania), Ruža Tomašić (Croatia), Jarosław Kalinowski (Poland), Brian Hayes (Ireland), Romana Tomc (Slovenia), Sophie Montel (Fance), Enrique Calvet Chambon (Spain), Rolandas Paksas (Lithuania), Cristian-Silviu Buşoi (Romania), Aldo Patriciello (Italy), Philippe De Backer (Belgium), Ivan Štefanec (Slovenia), Filiz Hyusmenova (Bulgaria), Neoklis Sylikiotis (Cyprus), Mara Bizzotto (Italy) and gathered the support of 123 Members of the European Parliament.. Written declaration, under Rule 136 of Parliaments Rules of Procedure, on Alzheimers disease. 1. Alzheimers disease is an incurable neurodegenerative disease of the brain tissue that causes progressive and irreversible loss of mental functions, including ...
Authors: Fakhran S, Yaeger K, Alhilali L.. Purpose:To evaluate white matter integrity in patients with mild traumatic brain injury (TBI) who did not have morphologic abnormalities at conventional magnetic resonance (MR) imaging with diffusion-tensor imaging to determine any relationship between patterns of white matter injury and severity of postconcussion symptoms.Materials and Methods:The institutional review board approved this study, with waiver of informed consent. Diffusion-tensor images from 64 consecutive patients with mild TBI obtained with conventional MR imaging were evaluated retrospectively. Fractional anisotropy (FA) maps were generated as a measure of white matter integrity. All patients underwent a neurocognitive evaluation. Correlations between skeletonized FA values in white matter, total concussion symptom score, and findings of sleep and wake disturbances were analyzed with regression analysis that used tract-based spatial statistics.Results:Total concussion symptom scores ...
Episodic memory is a core feature of Alzheimers disease (AD) and mild cognitive impairment (MCI). Impaired episodic memory in AD results from the dysfunction of an integrated network and involves both gray and white matter pathologies. We explored the neural correlates of episodic memory in AD, MCI and healthy aging by correlating a measure of episodic memory with hippocampal volume and fractional anisotropy (FA) and mean diffusivity (MD) of the cingulum and fornix. Episodic memory was associated with hippocampal volume and MD of the cingulum and fornix. In contrast, there were fewer significant associations between episodic memory and FA. These findings support a relationship between episodic memory and hippocampal circuitry, and suggest that MD is a more sensitive marker of decreased white matter integrity in the study of AD and MCI than FA. Furthermore, MD was significantly associated with hippocampal volume, indicating that white matter pathology is not completely independent of gray matter
BACKGROUND: Previous Cochrane reviews have considered the use of cholinesterase inhibitors in both Parkinsons disease with dementia (PDD) and dementia with Lewy bodies (DLB). The clinical features of DLB and PDD have much in common and are distinguished primarily on the basis of whether or not parkinsonism precedes dementia by more than a year. Patients with both conditions have particularly severe deficits in cortical levels of the neurotransmitter acetylcholine. Therefore, blocking its breakdown using cholinesterase inhibitors may lead to clinical improvement. OBJECTIVES: To assess the efficacy, safety and tolerability of cholinesterase inhibitors in dementia with Lewy bodies (DLB), Parkinsons disease with dementia (PDD), and cognitive impairment in Parkinsons disease falling short of dementia (CIND-PD) (considered as separate phenomena and also grouped together as Lewy body disease). SEARCH METHODS: The trials were identified from a search of ALOIS, the Specialised Register of the Cochrane

Saya Bukan Megan Fox: DementiaSaya Bukan Megan Fox: Dementia

Whipples disease Dementia of the Alzheimers Type Keadaan ini mula dikenalpasti oleh Alois Alzheimer pada tahun 1907. Diagnosa ... adalah lebih kerap dilihat pada Picks disease daripada Alzheimers disease.. Huntingtons Disease ... Parkinsons Disease. Seperti Huntingtons disease, parkinsonism adalah penyakit pada basal ganglia, dan kerap menunjukkan ... Senile plaques also referred as amyloid plaques, are more indicative of Alzheimers disease, although they are also seen in ...
more infohttp://cathenclox.blogspot.com/2009/10/dementia.html

Alzheimers Association | Alzheimers Disease & Dementia HelpAlzheimer's Association | Alzheimer's Disease & Dementia Help

... information on Alzheimers disease and dementia symptoms, diagnosis, stages, treatment, care and support resources. ... A World Without Alzheimers Disease®. Formed in 1980, the Alzheimers Association is the leading voluntary health organization ... Understanding Alzheimers Disease. Alzheimers is the most common form of dementia. It causes problems with memory, thinking ... Americans are living with Alzheimers disease.. By 2050, this number is projected to rise to nearly. 14 MILLION.. Get the Facts ...
more infohttps://www.alz.org/

Alzheimers Brain Plaques - Alzheimers AssociationAlzheimer's Brain Plaques - Alzheimer's Association

... an interactive diagram of beta-amyloid formation and how they contribute to the development of plaques in the Alzheimers brain ... Alzheimers Disease and the Brain. 8 9 10 11 12 13 14 15 16 ... Alzheimers Association is a not-for-profit 501(c)(3) ... Stay up-to-date on advances in Alzheimers treatments, care & research. Get tips for living with Alzheimers. ... Alzheimers Association National Office, 225 N. Michigan Ave., Fl. 17, Chicago, IL 60601. ...
more infohttps://www.alz.org/braintour/plaques.asp

Alzheimers disease - NHSAlzheimer's disease - NHS

Alzheimers disease is the most common cause of dementia. Dementia is a group of symptoms associated with a decline in the way ... Read more about the causes of Alzheimers disease.. Signs and symptoms of Alzheimers disease. Alzheimers disease is a ... Read more about diagnosing Alzheimers disease.. How Alzheimers disease is treated. Theres currently no cure for Alzheimers ... Can Alzheimers disease be prevented?. As the exact cause of Alzheimers disease is not clear, theres no known way to prevent ...
more infohttps://www.nhs.uk/conditions/alzheimers-disease/

Alzheimers DiseaseAlzheimer's Disease

Researchers discover novel genes responsible for Alzheimers disease. *Lithium in drinking water can slow Alzheimers disease ... There is no cure for Alzheimers disease, but several medications may improve certain symptoms as well as slowing disease ... Alzheimers disease is the most common form of dementia and affects millions of individuals worldwide. Dementia is a medical ... The exact cause of Alzheimers disease is not known, but a number of factors are thought to increase the risk of developing the ...
more infohttps://www.news-medical.net/health/Alzheimers-Disease.aspx

Alzheimers DiseaseAlzheimer's Disease

Alzheimers disease is a progressive form of dementia that interferes with memory, thinking, and behavior. Learn how to ... Symptoms of Alzheimers disease. Everyone has episodes of forgetfulness from time to time. But people with Alzheimers disease ... Diagnosing Alzheimers disease. The only definitive way to diagnose someone with Alzheimers disease is to examine their brain ... Treating Alzheimers disease. Theres no known cure for Alzheimers disease. But your doctor can recommend medications and ...
more infohttps://www.healthline.com/health/alzheimers-disease?ref=global

Alzheimer Disease | MedscapeAlzheimer Disease | Medscape

... and guidelines on Alzheimer Disease. Recognize the causes of Alzheimer Disease and signs of Alzheimer Disease, including ... Alzheimer Disease : Review in-depth clinical information, latest medical news, ...
more infohttps://www.medscape.com/resource/alzheimers

Alzheimers disease | InfopleaseAlzheimer's disease | Infoplease

The disease is characterized by abnormal accumulation of plaques and by ... degenerative disease of nerve cells in the cerebral cortex that leads to atrophy of the brain and senile dementia and, ... Alzheimers disease. Alzheimers disease ăls´hī˝mərz, ôls- [key], degenerative disease of nerve cells in the cerebral cortex ... the disease is almost as significant as heart disease and cancer. The cause of Alzheimers is unknown, but a number of genes ...
more infohttps://www.infoplease.com/encyclopedia/medicine/diseases-and-conditions/pathology/alzheimers-disease

Alzheimers DiseaseAlzheimer's Disease

Alzheimers Disease. ​​Alzheimers disease is a type of dementia that causes problems with memory, thinking and behavior. ... Alzheimers disease accounts for 60 to 80 percent of dementia cases. Currently there is no cure for Alzheimers, but treatments ... Center for Chronic Disease Prevention and Health PromotionCurrently selected *Division of Chronic Disease and Injury Control * ... Although current Alzheimers treatments cannot stop the disease from progressing, they can temporarily slow the worsening of ...
more infohttps://www.cdph.ca.gov/Programs/CCDPHP/DCDIC/CDCB/Pages/AlzheimersDisease.aspx

Early-onset Alzheimers disease - WikipediaEarly-onset Alzheimer's disease - Wikipedia

Familial Alzheimers disease[edit]. Familial Alzheimers disease (FAD) or early-onset familial Alzheimers disease (EOFAD) is ... Early-onset Alzheimers disease, also called early-onset Alzheimers, or early-onset AD, is Alzheimers disease diagnosed ... History of Alzheimers disease[edit]. Main article: Alzheimers disease § History. The symptoms of the disease as a distinct ... "Familial Alzheimers disease in kindreds with missense mutations in a gene on chromosome 1 related to the Alzheimers disease ...
more infohttps://en.wikipedia.org/wiki/Familial_Alzheimer_disease

Early-onset Alzheimers disease - WikipediaEarly-onset Alzheimer's disease - Wikipedia

Familial Alzheimers disease[edit]. Familial Alzheimers disease (FAD) or early onset familial Alzheimers disease (EOFAD) is ... Early-onset Alzheimers disease, also called early-onset Alzheimers, or early-onset AD, is Alzheimers disease diagnosed ... History of Alzheimers disease[edit]. Main article: Alzheimers disease § History. The symptoms of the disease as a distinct ... of all Alzheimers cases. Approximately 13% of the cases of early-onset Alzheimers are familial Alzheimers disease,[1] where ...
more infohttps://en.wikipedia.org/wiki/Early-onset_Alzheimer_disease

Alzheimers Disease TreatmentsAlzheimer's Disease Treatments

... there are medications that can prevent or slow down progression of the disease, as well as improving some symptoms of the ... While there is no cure for Alzheimers disease, ... Alzheimers disease can progress for around ten years but when ... While there is no cure for Alzheimers disease, there are medications that can prevent or slow down progression of the disease ... Alzheimers disease progresses slowly, with initial symptoms presenting as memory problems and confusion, for example, and then ...
more infohttps://www.news-medical.net/health/Alzheimers-Disease-Treatments.aspx

Alzheimers diseaseAlzheimer's disease

Alzheimers disease. Erik Lovaas erikl at ibg.uit.no Sat Nov 21 00:59:38 EST 1992 *Previous message: Alzheimers disease ... Alzheimers disease ,From: jdevlin at pollux.usc.edu (Joseph T. Devlin) ,Date: 19 Nov 92 23:57:08 GMT ,Keywords: Alzheimers, ... On the possible role of iron-induced free radical peroxidation in neural degeneration in Alzheimers disease. Ann.NY Acad.Sci. ... Blood activity of Cu/Zn superoxide dismutase, glutathione peroxidase and catalase in Alzheimers disease: A case-control study ...
more infohttp://www.bio.net/bionet/mm/ageing/1992-November/000327.html

Alzheimers Disease Research CenterAlzheimer's Disease Research Center

The UW Alzheimers Disease Research Center seeks to advance research in genetic risk, develop neuroimaging biomarkers for ... Alzheimers Disease Research Center - University of Washington An NIH-funded research resource center, associated with the UW ... Martin, the founder of the UW Alzheimers Disease Research Center. At age 90, he still studies the mechanisms of brain aging ... One mans creative quest to support Alzheimers disease research invites us to take a twirl through the science of brain ...
more infohttp://depts.washington.edu/mbwc/adrc/news/P10

Alzheimers Disease Research Center - University of WashingtonAlzheimer's Disease Research Center - University of Washington

The UW Alzheimers Disease Research Center seeks to advance research in genetic risk, develop neuroimaging biomarkers for ... Alzheimers Disease Research Center (ADRC), University of Washington. Research Cores. Administrative Core Thomas J. Grabowski, ... Alzheimers Disease Research Center - University of Washington An NIH-funded research resource center, associated with the UW ... Examination by trained medical personnel is required to ensure proper diagnosis and treatment of Alzheimers disease and other ...
more infohttp://depts.washington.edu/mbwc/adrc/

Alzheimers Disease SymptomsAlzheimer's Disease Symptoms

Alzheimers disease is a neurocognitive disorder (either major or minor, depending upon its severity) that has a subtle onset ... Alzheimers Disease Symptoms. By Steve Bressert, Ph.D. Last updated: 8 Sep 2018. ~ 1 min read ... Alzheimers disease is a neurocognitive disorder (either major or minor, depending upon its severity) that has a subtle onset ... The specific symptoms of Alzheimers disease are:. 1. The criteria are met for either major neurocognitive disorder or minor ...
more infohttps://psychcentral.com/disorders/alzheimers-disease-symptoms/

Alzheimers DiseaseAlzheimer's Disease

Further Alzheimers Disease Reading. *National Institute of Neurologic Diseases and Stroke Alzheimers Disease Information Page ... Alzheimers Disease Alzheimers disease is a gradually progressive illness of the brain. Usually the earliest symptom is short- ... Alzheimers Disease Research. *The Emory Alzheimers Disease Research Center funded by the National Institute of Aging ... Alzheimers Disease Treatments. Current treatments for Alzheimers disease are aimed at improving the memory system of the ...
more infohttps://www.emoryhealthcare.org/neurology/alzheimers.html

Alzheimers Disease: Living & CaregivingAlzheimer's Disease: Living & Caregiving

Alzheimers treatment and Alzheimers care go hand in hand. Theres no cure -- yet. But as youll see here, theres a lot that ... Living with Alzheimers disease means caring for the patient -- and caring for the caregiver. Heres how to manage both of ...
more infohttps://www.webmd.com/alzheimers/guide/alzheimers-disease-treatment-care

Alzheimers Disease - BeliefnetAlzheimer's Disease - Beliefnet

Beliefnet offers spiritual resources to help bolster your strength as an Alzheimers Disease caregiver, as well as insights on ... Can You Prevent Alzheimers Disease?. Alzheimers disease is the most common form of dementia affecting people of the ages 65 ... 9 Signs of Alzheimers You Shouldnt.... If you suspect you or a loved one may have Alzheimers disease, here are some red ... Gift Ideas for People with Alzheimers.... The Alzheimers Association and the Alzheimer Foundation of America provide several ...
more infohttp://www.beliefnet.com/wellness/health/physical-health/alzheimers.aspx

Alzheimer disease | pathology | Britannica.comAlzheimer disease | pathology | Britannica.com

Alzheimer disease, degenerative brain disorder that develops in mid-to-late adulthood. It results in a progressive and ... Alzheimer diseaseOverview of Alzheimer disease.. Contunico © ZDF Enterprises GmbH, Mainz. The disease was first described in ... human disease: Alzheimers disease. …definitive diagnosis can be made. Alzheimers disease is the most common form of dementia ... nervous system disease: Dementia. …common cause of dementia is Alzheimer disease. The disease is common in the elderly. The ...
more infohttps://www.britannica.com/science/Alzheimer-disease

Alzheimers Disease Fast Facts - CNNAlzheimer's Disease Fast Facts - CNN

Read CNNs Fast Facts on Alzheimers disease, a progressive brain disorder that leads to loss of memory and other intellectual ... Alzheimers disease is fatal and there is no cure. It is a slow-moving disease that starts with memory loss and ends with ... Early-onset Alzheimers Disease:. Early-onset Alzheimers is an uncommon form of dementia that strikes people younger than age ... Early-onset Alzheimers disease often runs in families.. Research:. March 9, 2014 - In a first-of-its-kind study, researchers ...
more infohttps://edition.cnn.com/2013/08/23/health/alzheimers-disease-fast-facts/index.html

Alzheimers disease beyond APOE | Nature GeneticsAlzheimer's disease beyond APOE | Nature Genetics

Two genome-wide association studies together report three new susceptibility loci for late-onset Alzheimers disease. CLU, ... Alzheimers disease susceptibility genes modify the risk of Parkinson disease and Parkinsons disease-associated cognitive ... Down syndrome, Alzheimer disease, and cerebral amyloid angiopathy: The complex triangle of brain amyloidosis *María Carmona‐ ... Translating Alzheimers disease-associated polymorphisms into functional candidates: a survey of IGAP genes and SNPs *Yuriko ...
more infohttps://www.nature.com/articles/ng1009-1047?error=cookies_not_supported&code=1710d5f7-9f01-4cf6-a4d6-d7b3a7c83334

Doggy Alzheimers Disease - DogsDoggy Alzheimer's Disease - Dogs

... memory loss and personality changes that are very similar to Alzheimer s Disease in humans. Don t assume that changes in your ... heart disease, cancer, diabetes, and a canine version of Alzheimers disease.. A medical condition known as canine Cognitive ... Doggy Alzheimers Disease. Guest Author - Sandy Moyer. Have you noticed changes in your aging dogs zest for life? Has she ... Like Alzheimers disease, the cause of Canine Cognitive Dysfunction is unknown, but physical evidence, found only in autopsies ...
more infohttp://www.bellaonline.com/articles/art25417.asp

CiteSeerX - Neuroimaging Alzheimers DiseaseCiteSeerX - Neuroimaging Alzheimer's Disease

The disease-specific features these atlases resolve can then be linked with demographic factors such as age, gender, handedness ... The disease-specific features these atlases resolve can then be linked with demographic factors such as age, gender, handedness ... disease-specific feature demographic factor different dementia subtypes dynamic data frontotemporal dementia semantic dementia ...
more infohttp://citeseerx.ist.psu.edu/viewdoc/summary?doi=10.1.1.7.2732

Microglia in Alzheimers DiseaseMicroglia in Alzheimer's Disease

... in Alzheimers disease," Neurodegenerative Diseases, vol. 3, no. 6, pp. 313-319, 2007. View at Publisher · View at Google ... "Say NO to Alzheimers disease: the putative links between nitric oxide and dementia of the Alzheimers type," Brain Research ... Microglia in Alzheimers Disease. Ying Li,1,2 Meng-Shan Tan,3 Teng Jiang,4 and Lan Tan1,3,4 ... Y. J. Lee, S. B. Han, S. Y. Nam, K. W. Oh, and J. T. Hong, "Inflammation and Alzheimers disease," Archives of Pharmacal ...
more infohttps://www.hindawi.com/journals/bmri/2014/437483/ref/
  • The idea that amyloid beta serves as a natural antibiotic implies that Alzheimer disease may be in some way linked to brain infection, plaque formation being either excessive in older individuals or abnormal in some other way in persons who eventually develop Alzheimer disease. (britannica.com)
  • The most important clinical research is focused on potentially treating the underlying disease pathology, for which reduction of amyloid beta is a common target of compounds under investigation. (wikipedia.org)
  • There are three recognized stages of Alzheimer disease: preclinical, mild cognitive impairment (MCI), and Alzheimer dementia. (britannica.com)
  • Dr. John Morris of Washington University School of Medicine in St. Louis, Missouri, published a report titled "Tangles and plaques in nondemented aging and preclinical Alzheimer's disease" in the March 1999 issue of Annals of Neurology , Volume 45 Number 3, pages 358-368. (washington.edu)
  • 5. Recent special issues:  Propagation of Tau Pathology (Guest Editors: Miguel Medina and Jesus Avila)  Proceedings of the IX Sindem Meeting  2013 International Congress on Vascular Dementia (Guest Editor: Amos D. Korczyn)  Alzheimer's Disease: Detection, Prevention, and Preclinical Treatment (Guest Editor: Jack C. de la Torre)  Volume 44:3 - Our 200th Issue! (slideshare.net)
  • The underlying neurobiology of this disease is just recently starting to be understood. (wikipedia.org)
  • A condition called mild cognitive impairment, in which a person experiences an inability to form memories for events that occurred a few minutes ago, typically is the first sign of the disease. (infoplease.com)
  • These drugs have been shown to benefit patients with mild-to-moderate disease and some studies suggest a benefit for those with advanced disease. (news-medical.net)
  • The disease-specific features these atlases resolve can then be linked with demographic factors such as age, gender, handedness, as well as specific clinical or genetic parameters (Mazziotta et al. (psu.edu)
  • In April 2014 there were 315 open clinical trials under way to understand and treat Alzheimer's disease. (wikipedia.org)
  • A gamma secretase inhibitor, semagacestat, failed to show any benefit to Alzheimer's disease patients in clinical trials. (wikipedia.org)
  • Notes : By analogy to the etiology of the pneumoconioses, exogenous dust-induced diseases of the lung, and endogenous crystal- induced arthropathies such as gout, it is proposed that Alzheimer's dementia and allied disorders are causally related to the accumulation of fibriform inorganic deposits within the brain. (bio.net)
  • Ccr2 deficiency impairs microglial accumulation and accelerates progression of Alzheimer-like disease," Nature Medicine , vol. 13, no. 4, pp. 432-438, 2007. (hindawi.com)
  • Family history - Genetics play a role in an individual's risk of developing the disease. (cnn.com)
  • Not-for-profit organization working nationwide to improve the quality of life for Canadians affected by Alzheimer's disease and other dementias, and to advance research for the cause and cure. (dmoztools.net)
  • The leading UK care and research charity for people with this disease and other dementias, their families and carers. (dmoztools.net)
  • In the Liva digital healthcare app, a patient is given a healthcare professional coach to help them change their lifestyle or live with their disease. (news-medical.net)