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)
A familial disorder marked by AMYLOID deposits in the walls of small and medium sized blood vessels of CEREBRAL CORTEX and MENINGES.
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.
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.
Bleeding into one or both CEREBRAL HEMISPHERES including the BASAL GANGLIA and the CEREBRAL CORTEX. It is often associated with HYPERTENSION and CRANIOCEREBRAL TRAUMA.
Accumulations of extracellularly deposited AMYLOID FIBRILS within tissues.
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)
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.
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.
Inflammation of blood vessels within the central nervous system. Primary vasculitis is usually caused by autoimmune or idiopathic factors, while secondary vasculitis is caused by existing disease process. Clinical manifestations are highly variable but include HEADACHE; SEIZURES; behavioral alterations; INTRACRANIAL HEMORRHAGES; TRANSIENT ISCHEMIC ATTACK; and BRAIN INFARCTION. (From Adams et al., Principles of Neurology, 6th ed, pp856-61)
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.
The arterial blood vessels supplying the CEREBRUM.
An acid dye used in testing for hydrochloric acid in gastric contents. It is also used histologically to test for AMYLOIDOSIS.
A homologous group of endogenous CYSTEINE PROTEINASE INHIBITORS. The cystatins inhibit most CYSTEINE ENDOPEPTIDASES such as PAPAIN, and other peptidases which have a sulfhydryl group at the active site.
A form of pneumoconiosis resulting from inhalation of iron in the mining dust or welding fumes.
Bleeding within the SKULL, including hemorrhages in the brain and the three membranes of MENINGES. The escape of blood often leads to the formation of HEMATOMA in the cranial epidural, subdural, and subarachnoid spaces.
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.
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.
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.
Pathological conditions of intracranial ARTERIES supplying the CEREBRUM. These diseases often are due to abnormalities or pathological processes in the ANTERIOR CEREBRAL ARTERY; MIDDLE CEREBRAL ARTERY; and POSTERIOR CEREBRAL ARTERY.
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.
The three membranes that cover the BRAIN and the SPINAL CORD. They are the dura mater, the arachnoid, and the pia mater.
Any of the tubular vessels conveying the blood (arteries, arterioles, capillaries, venules, and veins).
An extracellular cystatin subtype that is abundantly expressed in bodily fluids. It may play a role in the inhibition of interstitial CYSTEINE PROTEASES.
Proteins in the cerebrospinal fluid, normally albumin and globulin present in the ratio of 8 to 1. Increases in protein levels are of diagnostic value in neurological diseases. (Brain and Bannister's Clinical Neurology, 7th ed, p221)
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
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.
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.
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.
Postmortem examination of the body.
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)
Unsaturated hydrocarbons of the type Cn-H2n, indicated by the suffix -ene. (Grant & Hackh's Chemical Dictionary, 5th ed, p408)
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.
Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
An ACUTE PHASE REACTION protein present in low concentrations in normal sera, but found at higher concentrations in sera of older persons and in patients with AMYLOIDOSIS. It is the circulating precusor of amyloid A protein, which is found deposited in AA type AMYLOID FIBRILS.
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.
Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.
Beta-lactam antibiotics that differ from PENICILLINS in having the thiazolidine sulfur atom replaced by carbon, the sulfur then becoming the first atom in the side chain. They are unstable chemically, but have a very broad antibacterial spectrum. Thienamycin and its more stable derivatives are proposed for use in combinations with enzyme inhibitors.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
Death resulting from the presence of a disease in an individual, as shown by a single case report or a limited number of patients. This should be differentiated from DEATH, the physiological cessation of life and from MORTALITY, an epidemiological or statistical concept.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
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.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.

Intracellular accumulation of the amyloidogenic L68Q variant of human cystatin C in NIH/3T3 cells. (1/260)

AIM: To study the cellular transport of L68Q cystatin C, the cystatin variant causing amyloidosis and brain haemorrhage in patients suffering from hereditary cystatin C amyloid angiopathy (HCCAA). METHODS: Expression vectors for wild-type and L68Q cystatin C were constructed and used to transfect mouse NIH/3T3 cells. Stable cell clones were isolated after cotransfection with pSV2neo. Clones expressing human wild-type and L68Q cystatin C were compared with respect to secreted cystatin C by enzyme linked immunosorbent assay (ELISA), and for intracellular cystatin C by western blotting and immunofluorescence cytochemistry. Colocalisation studies in cells were performed by double staining with antibodies against human cystatin C and marker proteins for lysosomes, the Golgi apparatus, or the endoplasmic reticulum, and evaluated by confocal microscopy. RESULTS: Concentrations of human cystatin C secreted from transfected NIH/3T3 cells were similar to those secreted from human cells in culture. In general, clones expressing the gene encoding L68Q cystatin C secreted slightly lower amounts of the protein than clones expressing wild-type human cystatin C. Both immunofluorescence cytochemistry and western blotting experiments showed an increased accumulation of cystatin C in cells expressing the gene encoding L68Q cystatin C compared with cells expressing the gene for the wild-type protein. The intracellularly accumulating L68Q cystatin C was insoluble and located mainly in the endoplasmic reticulum. CONCLUSIONS: The cellular transport of human cystatin C is impeded by the pathogenic amino acid substitution Leu68-->Gln. The resulting intracellular accumulation and increased localised concentration of L68Q cystatin C might be an important event in the molecular pathophysiology of amyloid formation and brain haemorrhage in patients with HCCAA.  (+info)

Histopathologic analysis of foci of signal loss on gradient-echo T2*-weighted MR images in patients with spontaneous intracerebral hemorrhage: evidence of microangiopathy-related microbleeds. (2/260)

BACKGROUND AND PURPOSE: Patients with spontaneous intracerebral hemorrhage (ICH) frequently have small areas of signal loss on gradient-echo T2*-weighted MR images, which have been suggested to represent remnants of previous microbleeds. Our aim was to provide histopathologic support for this assumption and to clarify whether the presence and location of microbleeds were associated with microangiopathy. METHODS: We performed MR imaging and correlative histopathologic examination in 11 formalin-fixed brains of patients who had died of an ICH (age range, 45-90 years). RESULTS: Focal areas of signal loss on MR images were noted in seven brains. They were seen in a corticosubcortical location in six brains, in the basal ganglia/thalami in five, and infratentorially in three specimens. Histopathologic examination showed focal hemosiderin deposition in 21 of 34 areas of MR signal loss. No other corresponding abnormalities were found; however, hemosiderin deposits were noted without MR signal changes in two brains. All specimens with MR foci of signal loss showed moderate to severe fibrohyalinosis, and there was additional evidence of amyloid angiopathy in two of those brains. CONCLUSION: Small areas of signal loss on gradient echo T2*-weighted images indicate previous extravasation of blood and are related to bleeding-prone microangiopathy of different origins.  (+info)

Cerebral amyloid angiopathy-related hemorrhage. Interaction of APOE epsilon2 with putative clinical risk factors. (3/260)

BACKGROUND AND PURPOSE: Current evidence suggests that the apolipoprotein E (APOE for gene; apoE for protein) epsilon4 allele predisposes to cerebral amyloid angiopathy (CAA) whereas epsilon2 is associated with CAA-related hemorrhage (CAAH). The clinical risk factors for other forms of intracranial hemorrhage are a less-frequent feature of CAAH. In this study we examined potential clinical risk factors in patients with CAAH and assessed these with respect to APOE genotype. METHODS: Thirty-six patients were identified with a pathological diagnosis of CAAH. Clinical notes were reviewed to document age of hemorrhage onset, history of dementia, antiplatelet/anticoagulant medication, hypertension, minor head trauma, or transient neurological events. In a review of reported cases of CAAH, the frequency of these clinical features was also recorded. APOE genotypes were determined with use of polymerase chain reaction techniques. RESULTS: There were 24 women and 12 men; the mean age was 70.3 years. One third (n=12) had been taking antiplatelet medication, and a similar number were demented. Nine patients were hypertensive, and 4 had a history of recent minor head trauma. The relative frequency of each of these clinical features was similar to that in previous reports. Forty-four percent (16 of 36) possessed an epsilon2 allele. Antiplatelet or anticoagulant medication, hypertension, or minor head trauma were significantly more frequent antecedents of CAAH in epsilon2 carriers than in non-epsilon2 carriers (81% versus 35%, P=0.008), antiplatelet/anticoagulant medication in particular (P=0.038). CONCLUSIONS: Our findings suggest that antiplatelet or anticoagulant medication, hypertension, or minor head trauma are most likely to precipitate cerebral hemorrhage in patients with CAA who are also epsilon2 carriers. This may result from isoform-specific effects of apoE on the structure of amyloid-laden blood vessel walls.  (+info)

Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer's disease. (4/260)

We have characterized amyloid beta peptide (Abeta) concentration, Abeta deposition, paired helical filament formation, cerebrovascular amyloid angiopathy, apolipoprotein E (ApoE) allotype, and synaptophysin concentration in entorhinal cortex and superior frontal gyrus of normal elderly control (ND) patients, Alzheimer's disease (AD) patients, and high pathology control (HPC) patients who meet pathological criteria for AD but show no synapse loss or overt antemortem symptoms of dementia. The measures of Abeta deposition, Abeta-immunoreactive plaques with and without cores, thioflavin histofluorescent plaques, and concentrations of insoluble Abeta, failed to distinguish HPC from AD patients and were poor correlates of synaptic change. By contrast, concentrations of soluble Abeta clearly distinguished HPC from AD patients and were a strong inverse correlate of synapse loss. Further investigation revealed that Abeta40, whether in soluble or insoluble form, was a particularly useful measure for classifying ND, HPC, and AD patients compared with Abeta42. Abeta40 is known to be elevated in cerebrovascular amyloid deposits, and Abeta40 (but not Abeta42) levels, cerebrovascular amyloid angiopathy, and ApoE4 allele frequency were all highly correlated with each other. Although paired helical filaments in the form of neurofibrillary tangles or a penumbra of neurites surrounding amyloid cores also distinguished HPC from AD patients, they were less robust predictors of synapse change compared with soluble Abeta, particularly soluble Abeta40. Previous experiments attempting to relate Abeta deposition to the neurodegeneration that underlies AD dementia may have failed because they assayed the classical, visible forms of the molecule, insoluble neuropil plaques, rather than the soluble, unseen forms of the molecule.  (+info)

A deletion polymorphism of alpha(2)-macroglobulin gene and cerebral amyloid angiopathy. (5/260)

BACKGROUND AND PURPOSE: alpha(2)-Macroglobulin may be implicated in amyloid beta protein deposition. A deletion in the exon 18 splice acceptor of the alpha(2)-macroglobulin gene (A2M) has been reported to be associated with risk for Alzheimer's disease (AD). In search of genetic risk factors for cerebral amyloid angiopathy (CAA), we investigated association of the A2M deletion polymorphism with CAA. METHODS: The association between the severity of CAA and A2M deletion polymorphism was investigated in 178 autopsy cases of the elderly including 68 patients with AD. RESULTS: There was no significant difference in the severity of CAA between individuals with the A2M deletion allele and those without in the AD, non-AD, or total cases. Status for the epsilon4 allele of the apolipoprotein E gene did not influence the results. CONCLUSIONS: Our results suggest that the A2M deletion polymorphism may not be a definitive risk factor of CAA in the elderly, although further study with larger samples is necessary to confirm this.  (+info)

Neuronal overexpression of mutant amyloid precursor protein results in prominent deposition of cerebrovascular amyloid. (6/260)

Transgenic mice that overexpress mutant human amyloid precursor protein (APP) exhibit one hallmark of Alzheimer's disease pathology, namely the extracellular deposition of amyloid plaques. Here, we describe significant deposition of amyloid beta (Abeta) in the cerebral vasculature [cerebral amyloid angiopathy (CAA)] in aging APP23 mice that had striking similarities to that observed in human aging and Alzheimer's disease. Amyloid deposition occurred preferentially in arterioles and capillaries and within individual vessels showed a wide heterogeneity (ranging from a thin ring of amyloid in the vessel wall to large plaque-like extrusions into the neuropil). CAA was associated with local neuron loss, synaptic abnormalities, microglial activation, and microhemorrhage. Although several factors may contribute to CAA in humans, the neuronal origin of transgenic APP, high levels of Abeta in cerebrospinal fluid, and regional localization of CAA in APP23 mice suggest transport and drainage pathways rather than local production or blood uptake of Abeta as a primary mechanism underlying cerebrovascular amyloid formation. APP23 mice on an App-null background developed a similar degree of both plaques and CAA, providing further evidence that a neuronal source of APP/Abeta is sufficient to induce cerebrovascular amyloid and associated neurodegeneration.  (+info)

Novel presenilin-1 mutation with widespread cortical amyloid deposition but limited cerebral amyloid angiopathy. (7/260)

OBJECTIVE: To clarify the phenotypic heterogeneity in deposition of amyloid beta (Abeta) in the parenchyma and in cerebral vessels of the brains of the patients having presenilin-1 (PS1) mutations. Mutations in PS1 induce increased production of Abeta42(43), resulting in an enhanced overall deposition of Abeta protein within the cerebral cortex. METHODS: Sequence analysis of the PS1 gene of DNA from patients with early onset Alzheimer's disease, and immunostaining of brain tissues by end specific monoclonal antibodies against Abeta. RESULTS: Sequence analysis disclosed a novel mutation (N405S) in the PS1 gene in a Japanese patient with early-onset Alzheimer's disease. Postmortem examination of one patient with N405S showed limited cerebral amyloid angiopathy, whereas postmortem examination of another Japanese patient with Alzheimer's disease with the E184D mutation disclosed severe cerebral amyloid angiopathy. The brains of both patients showed widespread neuritic plaques, neurofibrillary tangles, and neuronal loss. Immunostaining showed that Abeta42 was predominant over Abeta40 in neuritic plaques in both patients, whereas Abeta40 was found to be predominant over Abeta42 in cerebral amyloid angiopathy in the patient with E184D. However, most cortical vessels of the patient with N405S were not reactive with either of the antibodies. CONCLUSION: The N405S mutation of PS1 is a major determinant of cortical Abeta deposition but not cerebral amyloid angiopathy in Alzheimer's disease.  (+info)

Apolipoprotein E genotype and the risk of recurrent lobar intracerebral hemorrhage. (8/260)

BACKGROUND: Recurrent lobar intracerebral hemorrhage is the hallmark of cerebral amyloid angiopathy. The factors that predispose patients to early recurrence of lobar hemorrhage are unknown. One candidate is the apolipoprotein E gene, since both the epsilon2 and the epsilon4 alleles of apolipoprotein E appear to be associated with the severity of amyloid angiopathy. METHODS: We performed a prospective, longitudinal study of consecutive elderly patients who survived a lobar intracerebral hemorrhage. The patients were followed for recurrent hemorrhagic stroke by interviews at six-month intervals and reviews of medical records and computed tomographic scans. RESULTS: Nineteen of 71 enrolled patients had recurrent hemorrhages during a mean follow-up period of 23.9+/-14.8 months, yielding a 2-year cumulative rate of recurrence of 21 percent. The apolipoprotein E genotype was significantly associated with the risk of recurrence. Carriers of the epsilon2 or epsilon4 allele had a two-year rate of recurrence of 28 percent, as compared with only 10 percent for patients with the common apolipoprotein E epsilon3/epsilon3 genotype (risk ratio, 3.8; 95 percent confidence interval, 1.2 to 11.6; P=0.01). Early recurrence occurred in eight patients, four of whom had the uncommon epsilon2/epsilon4 genotype. Also at increased risk for recurrence were patients with a history of hemorrhagic stroke before entry into the study (two-year recurrence, 61 percent; risk ratio, 6.4; 95 percent confidence interval, 2.2 to 18.5; P<0.001). CONCLUSIONS: The apolipoprotein E genotype can identify patients with lobar intracerebral hemorrhage who are at highest risk for early recurrence. This finding makes possible both the provision of prognostic information to patients with lobar hemorrhage and a method of targeting and assessing potential strategies for prevention.  (+info)

Cerebral amyloid angiopathy (CAA) is a medical condition characterized by the accumulation of beta-amyloid protein in the walls of small to medium-sized blood vessels in the brain. This protein buildup can cause damage to the vessel walls, leading to bleeding (cerebral hemorrhage), cognitive decline, and other neurological symptoms.

CAA is often associated with aging and is a common finding in older adults. It can also be seen in people with Alzheimer's disease and other forms of dementia. The exact cause of CAA is not fully understood, but it is believed to result from the abnormal processing and clearance of beta-amyloid protein in the brain.

The diagnosis of CAA typically involves a combination of clinical evaluation, imaging studies such as MRI or CT scans, and sometimes cerebrospinal fluid analysis. Treatment for CAA is generally supportive and focused on managing symptoms and preventing complications. There are currently no approved disease-modifying treatments for CAA.

Cerebral amyloid angiopathy (CAA), familial type, is a genetic disorder characterized by the buildup of beta-amyloid protein in the walls of blood vessels in the brain. This accumulation can lead to bleeding in the brain (cerebral hemorrhage) and cognitive decline. It is caused by mutations in genes associated with the production or clearance of beta-amyloid, such as the APP, PSEN1, and PSEN2 genes. These genetic mutations are typically inherited in an autosomal dominant manner, meaning that a child has a 50% chance of inheriting the mutation from a parent who carries it. The presence of these mutations leads to an increased production or decreased clearance of beta-amyloid, resulting in its accumulation in the blood vessel walls and subsequent complications.

Amyloid beta-peptides (Aβ) are small protein fragments that are crucially involved in the pathogenesis of Alzheimer's disease. They are derived from a larger transmembrane protein called the amyloid precursor protein (APP) through a series of proteolytic cleavage events.

The two primary forms of Aβ peptides are Aβ40 and Aβ42, which differ in length by two amino acids. While both forms can be harmful, Aβ42 is more prone to aggregation and is considered to be the more pathogenic form. These peptides have the tendency to misfold and accumulate into oligomers, fibrils, and eventually insoluble plaques that deposit in various areas of the brain, most notably the cerebral cortex and hippocampus.

The accumulation of Aβ peptides is believed to initiate a cascade of events leading to neuroinflammation, oxidative stress, synaptic dysfunction, and neuronal death, which are all hallmarks of Alzheimer's disease. Although the exact role of Aβ in the onset and progression of Alzheimer's is still under investigation, it is widely accepted that they play a central part in the development of this debilitating neurodegenerative disorder.

Amyloid is a term used in medicine to describe abnormally folded protein deposits that can accumulate in various tissues and organs of the body. These misfolded proteins can form aggregates known as amyloid fibrils, which have a characteristic beta-pleated sheet structure. Amyloid deposits can be composed of different types of proteins, depending on the specific disease associated with the deposit.

In some cases, amyloid deposits can cause damage to organs and tissues, leading to various clinical symptoms. Some examples of diseases associated with amyloidosis include Alzheimer's disease (where amyloid-beta protein accumulates in the brain), systemic amyloidosis (where amyloid fibrils deposit in various organs such as the heart, kidneys, and liver), and type 2 diabetes (where amyloid deposits form in the pancreas).

It's important to note that not all amyloid deposits are harmful or associated with disease. However, when they do cause problems, treatment typically involves managing the underlying condition that is leading to the abnormal protein accumulation.

A cerebral hemorrhage, also known as an intracranial hemorrhage or intracerebral hemorrhage, is a type of stroke that results from bleeding within the brain tissue. It occurs when a weakened blood vessel bursts and causes localized bleeding in the brain. This bleeding can increase pressure in the skull, damage nearby brain cells, and release toxic substances that further harm brain tissues.

Cerebral hemorrhages are often caused by chronic conditions like hypertension (high blood pressure) or cerebral amyloid angiopathy, which weakens the walls of blood vessels over time. Other potential causes include trauma, aneurysms, arteriovenous malformations, illicit drug use, and brain tumors. Symptoms may include sudden headache, weakness, numbness, difficulty speaking or understanding speech, vision problems, loss of balance, and altered level of consciousness. Immediate medical attention is required to diagnose and manage cerebral hemorrhage through imaging techniques, supportive care, and possible surgical interventions.

Amyloid plaque is a pathological hallmark of several degenerative diseases, including Alzheimer's disease. It refers to extracellular deposits of misfolded proteins that accumulate in various tissues and organs, but are most commonly found in the brain. The main component of these plaques is an abnormally folded form of a protein called amyloid-beta (Aβ). This protein is produced through the normal processing of the amyloid precursor protein (APP), but in amyloid plaques, it aggregates into insoluble fibrils that form the core of the plaque.

The accumulation of amyloid plaques is thought to contribute to neurodegeneration and cognitive decline in Alzheimer's disease and other related disorders. The exact mechanisms by which this occurs are not fully understood, but it is believed that the aggregation of Aβ into plaques leads to the disruption of neuronal function and viability, as well as the activation of inflammatory responses that can further damage brain tissue.

It's important to note that while amyloid plaques are a key feature of Alzheimer's disease, they are not exclusive to this condition. Amyloid plaques have also been found in other neurodegenerative disorders, as well as in some normal aging brains, although their significance in these contexts is less clear.

Alzheimer's disease is a progressive disorder that causes brain cells to waste away (degenerate) and die. It's the most common cause of dementia — a continuous decline in thinking, behavioral and social skills that disrupts a person's ability to function independently.

The early signs of the disease include forgetting recent events or conversations. As the disease progresses, a person with Alzheimer's disease will develop severe memory impairment and lose the ability to carry out everyday tasks.

Currently, there's no cure for Alzheimer's disease. However, treatments can temporarily slow the worsening of dementia symptoms and improve quality of life.

Amyloidosis is a medical condition characterized by the abnormal accumulation of insoluble proteins called amyloid in various tissues and organs throughout the body. These misfolded protein deposits can disrupt the normal function of affected organs, leading to a range of symptoms depending on the location and extent of the amyloid deposition.

There are different types of amyloidosis, classified based on the specific proteins involved:

1. Primary (AL) Amyloidosis: This is the most common form, accounting for around 80% of cases. It results from the overproduction and misfolding of immunoglobulin light chains, typically by clonal plasma cells in the bone marrow. The amyloid deposits can affect various organs, including the heart, kidneys, liver, and nervous system.
2. Secondary (AA) Amyloidosis: This form is associated with chronic inflammatory diseases, such as rheumatoid arthritis, tuberculosis, or familial Mediterranean fever. The amyloid fibrils are composed of serum amyloid A protein (SAA), an acute-phase reactant produced during the inflammatory response. The kidneys are commonly affected in this type of amyloidosis.
3. Hereditary or Familial Amyloidosis: These forms are caused by genetic mutations that result in the production of abnormal proteins prone to misfolding and amyloid formation. Examples include transthyretin (TTR) amyloidosis, fibrinogen amyloidosis, and apolipoprotein AI amyloidosis. These forms can affect various organs, including the heart, nerves, and kidneys.
4. Dialysis-Related Amyloidosis: This form is seen in patients undergoing long-term dialysis for chronic kidney disease. The amyloid fibrils are composed of beta-2 microglobulin, a protein that accumulates due to impaired clearance during dialysis. The joints and bones are commonly affected in this type of amyloidosis.

The diagnosis of amyloidosis typically involves a combination of clinical evaluation, imaging studies, and tissue biopsy with the demonstration of amyloid deposition using special stains (e.g., Congo red). Treatment depends on the specific type and extent of organ involvement and may include supportive care, medications to target the underlying cause (e.g., chemotherapy, immunomodulatory agents), and organ transplantation in some cases.

The brain is the central organ of the nervous system, responsible for receiving and processing sensory information, regulating vital functions, and controlling behavior, movement, and cognition. It is divided into several distinct regions, each with specific functions:

1. Cerebrum: The largest part of the brain, responsible for higher cognitive functions such as thinking, learning, memory, language, and perception. It is divided into two hemispheres, each controlling the opposite side of the body.
2. Cerebellum: Located at the back of the brain, it is responsible for coordinating muscle movements, maintaining balance, and fine-tuning motor skills.
3. Brainstem: Connects the cerebrum and cerebellum to the spinal cord, controlling vital functions such as breathing, heart rate, and blood pressure. It also serves as a relay center for sensory information and motor commands between the brain and the rest of the body.
4. Diencephalon: A region that includes the thalamus (a major sensory relay station) and hypothalamus (regulates hormones, temperature, hunger, thirst, and sleep).
5. Limbic system: A group of structures involved in emotional processing, memory formation, and motivation, including the hippocampus, amygdala, and cingulate gyrus.

The brain is composed of billions of interconnected neurons that communicate through electrical and chemical signals. It is protected by the skull and surrounded by three layers of membranes called meninges, as well as cerebrospinal fluid that provides cushioning and nutrients.

Vasculitis, Central Nervous System (CNS), refers to a group of disorders characterized by inflammation of blood vessels within the brain and/or spinal cord. This inflammation can cause damage to the blood vessel walls, leading to narrowing, blocking or weakening of the vessels, and in some cases, formation of aneurysms or rupture of the vessels.

The causes of CNS vasculitis are varied and can include infections, autoimmune diseases, medications, and unknown factors. The symptoms of CNS vasculitis depend on the severity and location of the inflammation, and may include headache, seizures, stroke-like symptoms (such as weakness or numbness in the face, arms, or legs), cognitive changes, and in severe cases, coma.

Diagnosis of CNS vasculitis typically involves a combination of clinical evaluation, imaging studies (such as MRI or angiography), and laboratory tests (including blood tests and analysis of cerebrospinal fluid). Treatment may involve corticosteroids, immunosuppressive medications, and/or other therapies aimed at reducing inflammation and preventing further damage to the blood vessels.

The Amyloid Beta-Protein Precursor (AβPP) is a type of transmembrane protein that is widely expressed in various tissues and organs, including the brain. It plays a crucial role in normal physiological processes, such as neuronal development, synaptic plasticity, and repair.

AβPP undergoes proteolytic processing by enzymes called secretases, resulting in the production of several protein fragments, including the amyloid-beta (Aβ) peptide. Aβ is a small peptide that can aggregate and form insoluble fibrils, which are the main component of amyloid plaques found in the brains of patients with Alzheimer's disease (AD).

The accumulation of Aβ plaques is believed to contribute to the neurodegeneration and cognitive decline observed in AD. Therefore, AβPP and its proteolytic processing have been the focus of extensive research aimed at understanding the pathogenesis of AD and developing potential therapies.

Cerebral arteries refer to the blood vessels that supply oxygenated blood to the brain. These arteries branch off from the internal carotid arteries and the vertebral arteries, which combine to form the basilar artery. The major cerebral arteries include:

1. Anterior cerebral artery (ACA): This artery supplies blood to the frontal lobes of the brain, including the motor and sensory cortices responsible for movement and sensation in the lower limbs.
2. Middle cerebral artery (MCA): The MCA is the largest of the cerebral arteries and supplies blood to the lateral surface of the brain, including the temporal, parietal, and frontal lobes. It is responsible for providing blood to areas involved in motor function, sensory perception, speech, memory, and vision.
3. Posterior cerebral artery (PCA): The PCA supplies blood to the occipital lobe, which is responsible for visual processing, as well as parts of the temporal and parietal lobes.
4. Anterior communicating artery (ACoA) and posterior communicating arteries (PComAs): These are small arteries that connect the major cerebral arteries, forming an important circulatory network called the Circle of Willis. The ACoA connects the two ACAs, while the PComAs connect the ICA with the PCA and the basilar artery.

These cerebral arteries play a crucial role in maintaining proper brain function by delivering oxygenated blood to various regions of the brain. Any damage or obstruction to these arteries can lead to serious neurological conditions, such as strokes or transient ischemic attacks (TIAs).

Congo Red is a synthetic diazo dye that is commonly used in histology and pathology for stainings and tests. It is particularly useful in identifying amyloid deposits in tissues, which are associated with various diseases such as Alzheimer's disease, type 2 diabetes, and systemic amyloidosis.

When Congo Red binds to amyloid fibrils, it exhibits a characteristic apple-green birefringence under polarized light microscopy. Additionally, Congo Red stained amyloid deposits show a shift in their emission spectrum when excited with circularly polarized light, a phenomenon known as dichroism. These properties make Congo Red a valuable tool for the diagnosis and study of amyloidosis and other protein misfolding disorders.

It is important to note that Congo Red staining should be performed with care, as it can be toxic and carcinogenic if not handled properly.

Cystatins are a group of proteins that inhibit cysteine proteases, which are enzymes that break down other proteins. Cystatins are found in various biological fluids and tissues, including tears, saliva, seminal plasma, and urine. They play an important role in regulating protein catabolism and protecting cells from excessive protease activity. There are three main types of cystatins: type 1 (cystatin C), type 2 (cystatin M, cystatin N, and fetuin), and type 3 (kininogens). Abnormal levels of cystatins have been associated with various pathological conditions, such as cancer, neurodegenerative diseases, and inflammatory disorders.

Siderosis is a medical condition characterized by the abnormal accumulation of iron in various tissues and organs, most commonly in the lungs. This occurs due to the repeated inhalation of iron-containing dusts or fumes, which can result from certain industrial processes such as welding, mining, or smelting.

In the lungs, this iron deposit can lead to inflammation and fibrosis, potentially causing symptoms like coughing, shortness of breath, and decreased lung function. It is important to note that siderosis itself is not contagious or cancerous, but there may be an increased risk for lung cancer in individuals with severe and prolonged exposure to iron-containing particles.

While siderosis is generally non-reversible, the progression of symptoms can often be managed through medical interventions and environmental modifications to reduce further exposure to iron-containing dusts or fumes.

Intracranial hemorrhage (ICH) is a type of stroke caused by bleeding within the brain or its surrounding tissues. It's a serious medical emergency that requires immediate attention and treatment. The bleeding can occur in various locations:

1. Epidural hematoma: Bleeding between the dura mater (the outermost protective covering of the brain) and the skull. This is often caused by trauma, such as a head injury.
2. Subdural hematoma: Bleeding between the dura mater and the brain's surface, which can also be caused by trauma.
3. Subarachnoid hemorrhage: Bleeding in the subarachnoid space, which is filled with cerebrospinal fluid (CSF) and surrounds the brain. This type of ICH is commonly caused by the rupture of an intracranial aneurysm or arteriovenous malformation.
4. Intraparenchymal hemorrhage: Bleeding within the brain tissue itself, which can be caused by hypertension (high blood pressure), amyloid angiopathy, or trauma.
5. Intraventricular hemorrhage: Bleeding into the brain's ventricular system, which contains CSF and communicates with the subarachnoid space. This type of ICH is often seen in premature infants but can also be caused by head trauma or aneurysm rupture in adults.

Symptoms of intracranial hemorrhage may include sudden severe headache, vomiting, altered consciousness, confusion, seizures, weakness, numbness, or paralysis on one side of the body, vision changes, or difficulty speaking or understanding speech. Rapid diagnosis and treatment are crucial to prevent further brain damage and potential long-term disabilities or death.

Apolipoprotein E (APOE) is a gene that provides instructions for making a protein involved in the metabolism of fats called lipids. One variant of this gene, APOE4, is associated with an increased risk of developing Alzheimer's disease and other forms of dementia.

The APOE4 allele (variant) is less efficient at clearing beta-amyloid protein, a component of the amyloid plaques found in the brains of people with Alzheimer's disease. This can lead to an accumulation of beta-amyloid and an increased risk of developing Alzheimer's disease.

It is important to note that having one or two copies of the APOE4 allele does not mean that a person will definitely develop Alzheimer's disease, but it does increase the risk. Other factors, such as age, family history, and the presence of other genetic variants, also contribute to the development of this complex disorder.

Neurofibrillary tangles are a pathological hallmark of several neurodegenerative disorders, most notably Alzheimer's disease. They are intracellular inclusions composed of abnormally phosphorylated and aggregated tau protein, which forms paired helical filaments. These tangles accumulate within the neurons, leading to their dysfunction and eventual death. The presence and density of neurofibrillary tangles are strongly associated with cognitive decline and disease progression in Alzheimer's disease and other related dementias.

Presenilin-1 (PSEN1) is a gene that provides instructions for making one part of an enzyme complex called gamma-secretase. This enzyme is involved in the breakdown of certain proteins, most notably the amyloid precursor protein (APP), into smaller fragments called peptides. One of these peptides, called beta-amyloid, can accumulate and form clumps called plaques, which are a characteristic feature of Alzheimer's disease.

Mutations in the PSEN1 gene have been identified as a major cause of early-onset familial Alzheimer's disease (FAD), a rare, inherited form of the disorder that usually develops before age 65. These mutations result in an abnormal gamma-secretase enzyme that produces more toxic beta-amyloid peptides and fewer harmless ones, leading to the formation of amyloid plaques and neurodegeneration.

It's important to note that while mutations in PSEN1 are associated with early-onset FAD, most cases of Alzheimer's disease are sporadic and develop later in life, typically after age 65. The role of PSEN1 and other genes associated with FAD in the more common, late-onset form of Alzheimer's is still being researched.

Cerebral arterial diseases refer to conditions that affect the blood vessels supplying the brain. These diseases can result in reduced blood flow, blockages, or bleeding in the brain. The most common cerebral arterial diseases include:

1. Atherosclerosis: A buildup of plaque made up of fat, cholesterol, and other substances in the inner lining of an artery, which can lead to narrowing or blockage of the artery.
2. Embolism: A blood clot or other particle that forms elsewhere in the body and travels to the brain, where it blocks a cerebral artery.
3. Thrombosis: The formation of a blood clot within a cerebral artery.
4. Aneurysm: A weakened area in the wall of an artery that bulges out and can rupture, causing bleeding in the brain.
5. Arteriovenous malformation (AVM): An abnormal tangle of blood vessels in the brain that can cause bleeding or reduced blood flow to surrounding tissue.
6. Vasculitis: Inflammation of the blood vessels in the brain, which can lead to narrowing, blockage, or weakening of the vessel walls.

These conditions can lead to serious complications such as stroke, transient ischemic attack (TIA), or vascular dementia. Treatment options include medications, surgery, and lifestyle changes to manage risk factors.

Apolipoprotein E (ApoE) is a protein involved in the metabolism of lipids, particularly cholesterol. It is produced primarily by the liver and is a component of several types of lipoproteins, including very low-density lipoproteins (VLDL) and high-density lipoproteins (HDL).

ApoE plays a crucial role in the transport and uptake of lipids in the body. It binds to specific receptors on cell surfaces, facilitating the delivery of lipids to cells for energy metabolism or storage. ApoE also helps to clear cholesterol from the bloodstream and is involved in the repair and maintenance of tissues.

There are three major isoforms of ApoE, designated ApoE2, ApoE3, and ApoE4, which differ from each other by only a few amino acids. These genetic variations can have significant effects on an individual's risk for developing certain diseases, particularly cardiovascular disease and Alzheimer's disease. For example, individuals who inherit the ApoE4 allele have an increased risk of developing Alzheimer's disease, while those with the ApoE2 allele may have a reduced risk.

In summary, Apolipoprotein E is a protein involved in lipid metabolism and transport, and genetic variations in this protein can influence an individual's risk for certain diseases.

The meninges are the protective membranes that cover the brain and spinal cord. They consist of three layers: the dura mater (the outermost, toughest layer), the arachnoid mater (middle layer), and the pia mater (the innermost, delicate layer). These membranes provide protection and support to the central nervous system, and contain blood vessels that supply nutrients and remove waste products. Inflammation or infection of the meninges is called meningitis, which can be a serious medical condition requiring prompt treatment.

Blood vessels are the part of the circulatory system that transport blood throughout the body. They form a network of tubes that carry blood to and from the heart, lungs, and other organs. The main types of blood vessels are arteries, veins, and capillaries. Arteries carry oxygenated blood away from the heart to the rest of the body, while veins return deoxygenated blood back to the heart. Capillaries connect arteries and veins and facilitate the exchange of oxygen, nutrients, and waste materials between the blood and the body's tissues.

Cystatin C is a protein produced by many cells in the body, including all types of nucleated cells. It is a member of the cysteine protease inhibitor family and functions as an endogenous inhibitor of cathepsins, which are proteases involved in various physiological and pathological processes such as extracellular matrix degradation, antigen presentation, and cell death.

Cystatin C is freely filtered by the glomeruli in the kidneys and almost completely reabsorbed and catabolized by the proximal tubules. Therefore, its serum concentration is a reliable marker of glomerular filtration rate (GFR) and can be used to estimate kidney function.

Increased levels of cystatin C in the blood may indicate impaired kidney function or kidney disease, while decreased levels are less common and may be associated with hyperfiltration or overproduction of cystatin C. Measuring cystatin C levels can complement or supplement traditional methods for assessing kidney function, such as estimating GFR based on serum creatinine levels.

Cerebrospinal fluid (CSF) proteins refer to the proteins present in the cerebrospinal fluid, which is a clear, colorless fluid that surrounds and protects the brain and spinal cord. The protein concentration in the CSF is much lower than that in the blood, and it contains a specific set of proteins that are produced by the brain, spinal cord, and associated tissues.

The normal range for CSF protein levels is typically between 15-45 mg/dL, although this can vary slightly depending on the laboratory's reference range. An elevation in CSF protein levels may indicate the presence of neurological disorders such as meningitis, encephalitis, multiple sclerosis, or Guillain-Barre syndrome. Additionally, certain conditions such as spinal cord injury, brain tumors, or neurodegenerative diseases can also cause an increase in CSF protein levels.

Therefore, measuring CSF protein levels is an important diagnostic tool for neurologists to evaluate various neurological disorders and monitor disease progression. However, it's essential to interpret the results of CSF protein tests in conjunction with other clinical findings and laboratory test results to make an accurate diagnosis.

Transgenic mice are genetically modified rodents that have incorporated foreign DNA (exogenous DNA) into their own genome. This is typically done through the use of recombinant DNA technology, where a specific gene or genetic sequence of interest is isolated and then introduced into the mouse embryo. The resulting transgenic mice can then express the protein encoded by the foreign gene, allowing researchers to study its function in a living organism.

The process of creating transgenic mice usually involves microinjecting the exogenous DNA into the pronucleus of a fertilized egg, which is then implanted into a surrogate mother. The offspring that result from this procedure are screened for the presence of the foreign DNA, and those that carry the desired genetic modification are used to establish a transgenic mouse line.

Transgenic mice have been widely used in biomedical research to model human diseases, study gene function, and test new therapies. They provide a valuable tool for understanding complex biological processes and developing new treatments for a variety of medical conditions.

Cerebrovascular disorders are a group of medical conditions that affect the blood vessels of the brain. These disorders can be caused by narrowing, blockage, or rupture of the blood vessels, leading to decreased blood flow and oxygen supply to the brain. The most common types of cerebrovascular disorders include:

1. Stroke: A stroke occurs when a blood vessel in the brain becomes blocked or bursts, causing a lack of oxygen and nutrients to reach brain cells. This can lead to permanent damage or death of brain tissue.
2. Transient ischemic attack (TIA): Also known as a "mini-stroke," a TIA occurs when blood flow to the brain is temporarily blocked, often by a blood clot. Symptoms may last only a few minutes to a few hours and typically resolve on their own. However, a TIA is a serious warning sign that a full-blown stroke may occur in the future.
3. Aneurysm: An aneurysm is a weakened or bulging area in the wall of a blood vessel. If left untreated, an aneurysm can rupture and cause bleeding in the brain.
4. Arteriovenous malformation (AVM): An AVM is a tangled mass of abnormal blood vessels that connect arteries and veins. This can lead to bleeding in the brain or stroke.
5. Carotid stenosis: Carotid stenosis occurs when the carotid arteries, which supply blood to the brain, become narrowed or blocked due to plaque buildup. This can increase the risk of stroke.
6. Vertebrobasilar insufficiency: This condition occurs when the vertebral and basilar arteries, which supply blood to the back of the brain, become narrowed or blocked. This can lead to symptoms such as dizziness, vertigo, and difficulty swallowing.

Cerebrovascular disorders are a leading cause of disability and death worldwide. Risk factors for these conditions include age, high blood pressure, smoking, diabetes, high cholesterol, and family history. Treatment may involve medications, surgery, or lifestyle changes to reduce the risk of further complications.

Medical Definition:

Magnetic Resonance Imaging (MRI) is a non-invasive diagnostic imaging technique that uses a strong magnetic field and radio waves to create detailed cross-sectional or three-dimensional images of the internal structures of the body. The patient lies within a large, cylindrical magnet, and the scanner detects changes in the direction of the magnetic field caused by protons in the body. These changes are then converted into detailed images that help medical professionals to diagnose and monitor various medical conditions, such as tumors, injuries, or diseases affecting the brain, spinal cord, heart, blood vessels, joints, and other internal organs. MRI does not use radiation like computed tomography (CT) scans.

Dementia is a broad term that describes a decline in cognitive functioning, including memory, language, problem-solving, and judgment, severe enough to interfere with daily life. It is not a specific disease but rather a group of symptoms that may be caused by various underlying diseases or conditions. Alzheimer's disease is the most common cause of dementia, accounting for 60-80% of cases. Other causes include vascular dementia, Lewy body dementia, frontotemporal dementia, and Huntington's disease.

The symptoms of dementia can vary widely depending on the cause and the specific areas of the brain that are affected. However, common early signs of dementia may include:

* Memory loss that affects daily life
* Difficulty with familiar tasks
* Problems with language or communication
* Difficulty with visual and spatial abilities
* Misplacing things and unable to retrace steps
* Decreased or poor judgment
* Withdrawal from work or social activities
* Changes in mood or behavior

Dementia is a progressive condition, meaning that symptoms will gradually worsen over time. While there is currently no cure for dementia, early diagnosis and treatment can help slow the progression of the disease and improve quality of life for those affected.

An autopsy, also known as a post-mortem examination or obduction, is a medical procedure in which a qualified professional (usually a pathologist) examines a deceased person's body to determine the cause and manner of death. This process may involve various investigative techniques, such as incisions to study internal organs, tissue sampling, microscopic examination, toxicology testing, and other laboratory analyses. The primary purpose of an autopsy is to gather objective evidence about the medical conditions and factors contributing to the individual's demise, which can be essential for legal, insurance, or public health purposes. Additionally, autopsies can provide valuable insights into disease processes and aid in advancing medical knowledge.

Vascular dementia is a type of dementia that is caused by damage to the blood vessels that supply blood to the brain. This damage can result from conditions such as stroke, chronic high blood pressure, diabetes, or other diseases that affect the circulatory system. The interruption in blood flow to the brain can lead to damaged or dead brain cells, which can impair cognitive function and cause symptoms similar to those seen in other types of dementia, such as Alzheimer's disease.

The symptoms of vascular dementia can vary depending on the severity and location of the damage to the blood vessels. However, common symptoms include difficulties with memory, attention, and decision-making; problems with language and speech; changes in mood or behavior; and difficulty walking or performing other physical tasks. Vascular dementia is typically a progressive condition, meaning that the symptoms tend to worsen over time.

It's important to note that vascular dementia can coexist with other types of dementia, such as Alzheimer's disease, and this is known as mixed dementia. Proper diagnosis and management of underlying medical conditions that contribute to vascular dementia can help slow down the progression of cognitive decline and improve quality of life for individuals living with this condition.

Alkenes are unsaturated hydrocarbons that contain at least one carbon-carbon double bond in their molecular structure. The general chemical formula for alkenes is CnH2n, where n represents the number of carbon atoms in the molecule.

The double bond in alkenes can undergo various reactions, such as addition reactions, where different types of molecules can add across the double bond to form new compounds. The relative position of the double bond in the carbon chain and the presence of substituents on the carbon atoms can affect the physical and chemical properties of alkenes.

Alkenes are important industrial chemicals and are used as starting materials for the synthesis of a wide range of products, including plastics, resins, fibers, and other chemicals. They are also found in nature, occurring in some plants and animals, and can be produced by certain types of bacteria through fermentation processes.

Apolipoprotein E2 (ApoE2) is one of the three major isoforms of the apolipoprotein E (ApoE) protein, which is a component of lipoproteins that are involved in the transport and metabolism of cholesterol and other fats in the body. ApoE is produced by the APOE gene, which has three common alleles: ε2, ε3, and ε4.

The ApoE2 protein is encoded by the ε2 allele of the APOE gene. Compared to the other two isoforms (ApoE3 and ApoE4), ApoE2 has a different amino acid at position 112, where it has a cysteine instead of an arginine. This difference affects the protein's ability to interact with other molecules involved in lipid metabolism, such as the low-density lipoprotein receptor (LDLR).

Individuals who inherit two copies of the ε2 allele (ε2/ε2) have a higher risk of developing type III hyperlipoproteinemia, also known as dysbetalipoproteinemia, which is characterized by elevated levels of cholesterol and triglycerides in the blood due to impaired clearance of remnant lipoproteins. However, not all people with the ε2/ε2 genotype develop type III hyperlipoproteinemia, and other genetic and environmental factors may contribute to the development of this condition.

It's worth noting that having one or two copies of the ε2 allele has been associated with a reduced risk of developing Alzheimer's disease, although the mechanism by which ApoE2 protects against Alzheimer's is not fully understood.

A peptide fragment is a short chain of amino acids that is derived from a larger peptide or protein through various biological or chemical processes. These fragments can result from the natural breakdown of proteins in the body during regular physiological processes, such as digestion, or they can be produced experimentally in a laboratory setting for research or therapeutic purposes.

Peptide fragments are often used in research to map the structure and function of larger peptides and proteins, as well as to study their interactions with other molecules. In some cases, peptide fragments may also have biological activity of their own and can be developed into drugs or diagnostic tools. For example, certain peptide fragments derived from hormones or neurotransmitters may bind to receptors in the body and mimic or block the effects of the full-length molecule.

Cerebrovascular circulation refers to the network of blood vessels that supply oxygenated blood and nutrients to the brain tissue, and remove waste products. It includes the internal carotid arteries, vertebral arteries, circle of Willis, and the intracranial arteries that branch off from them.

The internal carotid arteries and vertebral arteries merge to form the circle of Willis, a polygonal network of vessels located at the base of the brain. The anterior cerebral artery, middle cerebral artery, posterior cerebral artery, and communicating arteries are the major vessels that branch off from the circle of Willis and supply blood to different regions of the brain.

Interruptions or abnormalities in the cerebrovascular circulation can lead to various neurological conditions such as stroke, transient ischemic attack (TIA), and vascular dementia.

Serum Amyloid A (SAA) protein is an acute phase protein produced primarily in the liver, although it can also be produced by other cells in response to inflammation. It is a member of the apolipoprotein family and is found in high-density lipoproteins (HDL) in the blood. SAA protein levels increase rapidly during the acute phase response to infection, trauma, or tissue damage, making it a useful biomarker for inflammation.

In addition to its role as an acute phase protein, SAA has been implicated in several disease processes, including atherosclerosis and amyloidosis. In amyloidosis, SAA can form insoluble fibrils that deposit in various tissues, leading to organ dysfunction. There are four subtypes of SAA in humans (SAA1, SAA2, SAA3, and SAA4), with SAA1 and SAA2 being the most responsive to inflammatory stimuli.

The cerebral cortex is the outermost layer of the brain, characterized by its intricate folded structure and wrinkled appearance. It is a region of great importance as it plays a key role in higher cognitive functions such as perception, consciousness, thought, memory, language, and attention. The cerebral cortex is divided into two hemispheres, each containing four lobes: the frontal, parietal, temporal, and occipital lobes. These areas are responsible for different functions, with some regions specializing in sensory processing while others are involved in motor control or associative functions. The cerebral cortex is composed of gray matter, which contains neuronal cell bodies, and is covered by a layer of white matter that consists mainly of myelinated nerve fibers.

Brain diseases, also known as neurological disorders, refer to a wide range of conditions that affect the brain and nervous system. These diseases can be caused by various factors such as genetics, infections, injuries, degeneration, or structural abnormalities. They can affect different parts of the brain, leading to a variety of symptoms and complications.

Some examples of brain diseases include:

1. Alzheimer's disease - a progressive degenerative disorder that affects memory and cognitive function.
2. Parkinson's disease - a movement disorder characterized by tremors, stiffness, and difficulty with coordination and balance.
3. Multiple sclerosis - a chronic autoimmune disease that affects the nervous system and can cause a range of symptoms such as vision loss, muscle weakness, and cognitive impairment.
4. Epilepsy - a neurological disorder characterized by recurrent seizures.
5. Brain tumors - abnormal growths in the brain that can be benign or malignant.
6. Stroke - a sudden interruption of blood flow to the brain, which can cause paralysis, speech difficulties, and other neurological symptoms.
7. Meningitis - an infection of the membranes surrounding the brain and spinal cord.
8. Encephalitis - an inflammation of the brain that can be caused by viruses, bacteria, or autoimmune disorders.
9. Huntington's disease - a genetic disorder that affects muscle coordination, cognitive function, and mental health.
10. Migraine - a neurological condition characterized by severe headaches, often accompanied by nausea, vomiting, and sensitivity to light and sound.

Brain diseases can range from mild to severe and may be treatable or incurable. They can affect people of all ages and backgrounds, and early diagnosis and treatment are essential for improving outcomes and quality of life.

Thienamycins are a group of antibiotics that are characterized by their beta-lactam structure. They belong to the class of carbapenems and are known for their broad-spectrum antibacterial activity against both gram-positive and gram-negative bacteria, including many that are resistant to other antibiotics. Thienamycins inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins (PBPs), which leads to bacterial cell death.

Thienamycin itself is not used clinically due to its instability, but several semi-synthetic derivatives of thienamycin have been developed and are used in the treatment of serious infections caused by multidrug-resistant bacteria. Examples of thienamycin derivatives include imipenem, meropenem, and ertapenem. These antibiotics are often reserved for the treatment of severe infections that are unresponsive to other antibiotics due to their potential to select for resistant bacteria and their high cost.

Aging is a complex, progressive and inevitable process of bodily changes over time, characterized by the accumulation of cellular damage and degenerative changes that eventually lead to increased vulnerability to disease and death. It involves various biological, genetic, environmental, and lifestyle factors that contribute to the decline in physical and mental functions. The medical field studies aging through the discipline of gerontology, which aims to understand the underlying mechanisms of aging and develop interventions to promote healthy aging and extend the human healthspan.

A fatal outcome is a term used in medical context to describe a situation where a disease, injury, or illness results in the death of an individual. It is the most severe and unfortunate possible outcome of any medical condition, and is often used as a measure of the severity and prognosis of various diseases and injuries. In clinical trials and research, fatal outcome may be used as an endpoint to evaluate the effectiveness and safety of different treatments or interventions.

Immunohistochemistry (IHC) is a technique used in pathology and laboratory medicine to identify specific proteins or antigens in tissue sections. It combines the principles of immunology and histology to detect the presence and location of these target molecules within cells and tissues. This technique utilizes antibodies that are specific to the protein or antigen of interest, which are then tagged with a detection system such as a chromogen or fluorophore. The stained tissue sections can be examined under a microscope, allowing for the visualization and analysis of the distribution and expression patterns of the target molecule in the context of the tissue architecture. Immunohistochemistry is widely used in diagnostic pathology to help identify various diseases, including cancer, infectious diseases, and immune-mediated disorders.

Animal disease models are specialized animals, typically rodents such as mice or rats, that have been genetically engineered or exposed to certain conditions to develop symptoms and physiological changes similar to those seen in human diseases. These models are used in medical research to study the pathophysiology of diseases, identify potential therapeutic targets, test drug efficacy and safety, and understand disease mechanisms.

The genetic modifications can include knockout or knock-in mutations, transgenic expression of specific genes, or RNA interference techniques. The animals may also be exposed to environmental factors such as chemicals, radiation, or infectious agents to induce the disease state.

Examples of animal disease models include:

1. Mouse models of cancer: Genetically engineered mice that develop various types of tumors, allowing researchers to study cancer initiation, progression, and metastasis.
2. Alzheimer's disease models: Transgenic mice expressing mutant human genes associated with Alzheimer's disease, which exhibit amyloid plaque formation and cognitive decline.
3. Diabetes models: Obese and diabetic mouse strains like the NOD (non-obese diabetic) or db/db mice, used to study the development of type 1 and type 2 diabetes, respectively.
4. Cardiovascular disease models: Atherosclerosis-prone mice, such as ApoE-deficient or LDLR-deficient mice, that develop plaque buildup in their arteries when fed a high-fat diet.
5. Inflammatory bowel disease models: Mice with genetic mutations affecting intestinal barrier function and immune response, such as IL-10 knockout or SAMP1/YitFc mice, which develop colitis.

Animal disease models are essential tools in preclinical research, but it is important to recognize their limitations. Differences between species can affect the translatability of results from animal studies to human patients. Therefore, researchers must carefully consider the choice of model and interpret findings cautiously when applying them to human diseases.

Microcirculation is the circulation of blood in the smallest blood vessels, including arterioles, venules, and capillaries. It's responsible for the delivery of oxygen and nutrients to the tissues and the removal of waste products. The microcirculation plays a crucial role in maintaining tissue homeostasis and is regulated by various physiological mechanisms such as autonomic nervous system activity, local metabolic factors, and hormones.

Impairment of microcirculation can lead to tissue hypoxia, inflammation, and organ dysfunction, which are common features in several diseases, including diabetes, hypertension, sepsis, and ischemia-reperfusion injury. Therefore, understanding the structure and function of the microcirculation is essential for developing new therapeutic strategies to treat these conditions.

... (CAA) is a form of angiopathy in which amyloid beta peptide deposits in the walls of small to ... The aim in cerebral amyloid angiopathy is to treat the symptoms, as there is no current cure. Physical, occupational and/or ... Cerebral amyloid angiopathy can be presented with lobar intracerebral hemorrhage or microbleeds in the brain. The bleeding ... "Cerebral amyloid angiopathy: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-05-27. "UpToDate". www.uptodate ...
"Cerebral amyloid angiopathy without and with cerebral hemorrhages: A comparative histological study". Annals of Neurology. 30 ( ... The Boston criteria version 2.0 is a set of guidelines designed to diagnose cerebral amyloid angiopathy (CAA), a disease that ... Schroeder, B. E.; Robertson, N. P.; Hughes, T. A. T. (2023-03-24). "Cerebral amyloid angiopathy: an update". Journal of ... Vinters, H V (March 1987). "Cerebral amyloid angiopathy. A critical review". Stroke. 18 (2): 311-324. doi:10.1161/01.str.18.2. ...
VLDLR Cerebral amyloid angiopathy; 105150; CST3 Cerebral amyloid angiopathy, Dutch, Italian, Iowa, Flemish, Arctic variants; ... SNAP29 Cerebral palsy, spastic quadriplegic, 3; 612936; AP4M1 Cerebral palsy, spastic quadriplegic; 612900; KANK1 Cerebral ... NOTCH3 Cerebral cavernous malformations 3; 603285; PDCD10 Cerebral cavernous malformations-1; 116860; CCM1 Cerebral cavernous ... C1NH Angiopathy, hereditary, with nephropathy, aneurysms, and muscle cramps; 611773; COL4A1 Aniridia; 106210; PAX6 Anonychia ...
Cerebral amyloid angiopathy in this disorder is severe. CAA is present in all regions of the central nervous system. Other ... "Hereditary cerebral amyloid angiopathy: MedlinePlus Genetics". medlineplus.gov. Retrieved 2021-09-07. Dickson, Dennis; Weller, ... FDD is one of the two types of hereditary, cerebral amyloid angiopathy, alongside familial British dementia. Vision problems ... Histopathologically FDD was characterized by severe cerebral amyloid angiopathy with neurofibrillary tangle deposition in the ...
Down syndrome or cerebral amyloid angiopathy. However, this has not been studied so far. No safety concerns were detected in ... Amyloid beta plaques mostly consist of amyloid beta42. Solanezumab binds free amyloid beta which causes amyloid beta42 to ... Plasma amyloid beta levels increased dose dependently over the course of treatment. In the cerebrospinal fluid amyloid beta40 ... Other anti-amyloid beta antibodies caused amyloid-related imaging abnormalities, which is not the case for solanezumab. ...
Such pathologies are arteriosclerosis or cerebral amyloid angiopathy. Microinfarcts take longer to affect neuronal death ... "Cerebral Microinfarcts: The Invisible Lesions." Lancet Neurology 11.3 (2012): 272-282. PMC. Web. 20 Mar. 2016. Wang M, Iliff JJ ... Retrieved September 1, 2014 Smith, Eric E.; Schneider, Julie A.; Wardlaw, Joanna M.; Greenberg, Steven M. (2012). "Cerebral ...
"Matrix metalloproteinase-9 in cerebral-amyloid-angiopathy-related hemorrhage". Journal of the Neurological Sciences. 229-230: ... Journal of Cerebral Blood Flow and Metabolism. 37 (1): 39-51. doi:10.1177/0271678X15625351. PMC 5363749. PMID 26746866. Ram M, ...
2007). "Imaging Cerebral Amyloid Angiopathy with Susceptibility-Weighted Imaging". American Journal of Neuroradiology. 28 (2): ... 2009). "Pneumocephalus mimicking cerebral cavernous malformations in MR susceptibility-weighted imaging". AJNR Am J Neuroradiol ... 2008). "Susceptibility-weighted imaging for the evaluation of patients with familial cerebral cavernous malformations: a ...
Levy E, Jaskolski M, Grubb A (January 2006). "The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology ... "Entrez Gene: CST3 cystatin C (amyloid angiopathy and cerebral hemorrhage)". Hwang SJ, Yang Q, Meigs JB, Pearce EN, Fox CS ( ... Mutations in the cystatin 3 gene are responsible for the Icelandic type of hereditary cerebral amyloid angiopathy, a condition ... "Stroke in Icelandic patients with hereditary amyloid angiopathy is related to a mutation in the cystatin C gene, an inhibitor ...
In another more recent case, an 80-year-old woman had been diagnosed with Cerebral Amyloid Angiopathy (CAA) and was described ... "Steroid-Responsive Recurrent Encephalopathy in a Patient with Cerebral Amyloid Angiopathy". Cerebrovascular Diseases. 23 (1): ...
"Intravenous injection of beta-amyloid seeds promotes cerebral amyloid angiopathy (CAA)". Acta Neuropathologica Communications. ... 2D cultures often have difficulties producing insoluble Amyloid-β plaques even when they are able to secrete the Amyloid-β ... "Intravenously Injected Amyloid-β Peptide With Isomerized Asp7 and Phosphorylated Ser8 Residues Inhibits Cerebral β-Amyloidosis ... These compounds include: Amyloid-β 42, tau protein, glutamic acid, and oxidative/pro-inflammatory compounds. Primary neuron ...
... intracerebral hemorrhage and cerebral amyloid angiopathy. He published more than 300 peer-reviewed article on those topics and ... "The increasing impact of cerebral amyloid angiopathy: essential new insights for clinical practice". Journal of Neurology, ... Wilson, D; Ambler, G; Lee, K-J; et, al; Werring, DJ (2019). "Cerebral microbleeds and stroke risk after ischaemic stroke or ... Cerebral microbleeds and intracranial haemorrhage risk in patients anticoagulated for atrial fibrillation after acute ischaemic ...
ABC transporters P-gp and BCRP are reduced in capillary cerebral amyloid angiopathy . Neurobiol Aging . 2014; 35: 565-75 ... Elected President of the International Brain Barrier Society 2011 Chair of Cerebral Vascular Biology Meeting in Leiden Troletti ... she was the chair of the 2011 Cerebral Vascular Biology Meeting held in Leiden, The Netherlands, and in 2013 she was elected to ...
"APP duplication is sufficient to cause early onset Alzheimer's dementia with cerebral amyloid angiopathy". Brain. 129 (Pt 11): ... "APP locus duplication causes autosomal dominant early-onset Alzheimer disease with cerebral amyloid angiopathy". Nature ... that have an extra copy of APP gene due to the locus duplication show Alzheimer's with severe cerebral amyloid angiopathy. G- ... Duplication in Amyloid precursor protein (APP) locus (duplicated segment varies in length but includes APP) on Chromosome 21 ...
"Reducing Available Soluble A-Amyloid Prevents Progression of Cerebral Amyloid Angiopathy in Transgenic Mice". J Neuropathol Exp ... Ray, Indrani; Chauhan, Abha; Wegiel, Jerzy; Chauhan, Ved P.S. (2000-01-24). "Gelsolin inhibits the fibrillization of amyloid ... to Amyloid β-Protein". Biochemical and Biophysical Research Communications. 258 (2): 241-6. doi:10.1006/bbrc.1999.0623. PMID ... "Peripheral Transgene Expression of Plasma Gelsolin Reduces Amyloid in Transgenic Mouse Models of Alzheimer's Disease". ...
Mutations in the 3' UTR of the APP gene are related to development of cerebral amyloid angiopathy. Through the recent study of ... "Mutation in the 3'untranslated region of APP as a genetic determinant of cerebral amyloid angiopathy". European Journal of ...
Levy, E; Jaskolski, M; Grubb, A (January 2006). "The role of cystatin C in cerebral amyloid angiopathy and stroke: cell biology ... Mutations in the cystatin 3 gene are responsible for the Icelandic type of hereditary cerebral amyloid angiopathy, a condition ... Hereditary cystatin C amyloid angiopathy (HCCAA) is a rare, fatal amyloid disease in young people in Iceland caused by a ... A, Palsdottir; Ao, Snorradottir; L, Thorsteinsson (January 2006). "Hereditary cystatin C amyloid angiopathy: genetic, clinical ...
... which may also reduce the risk of cerebral amyloid angiopathy and microbleeds (Poels et al., 2010). Howe TE, Rochester L, Neil ... Enhanced cerebral perfusion may not only facilitate the delivery of energy substrates, but also lower the risk of vascular- ... "Cerebral hemodynamics of the aging brain: risk of Alzheimer disease and benefit of aerobic exercise". Frontiers in Physiology. ... Cognitive decline in AD is attributable at least in part to the buildup of amyloid and tau proteins, which promote neuronal ...
"Vascular Pathology in Alzheimer Disease: Correlation of Cerebral Amyloid Angiopathy and Arteriosclerosis/Lipohyalinosis with ... cerebral amyloid angiopathy] and [arteriosclerosis/lipohyalinosis] may play a critical role in the development of [Alzheimer ... "Cerebral Small Vessel Disease: Capillary Pathways to Stroke and Cognitive Decline." Journal of Cerebral Blood Flow & Metabolism ... Cerebral small vessel disease is a major cause of cognitive decline in the older populations. The results from a small pilot ...
... may be primarily vascular, as in cerebral amyloid angiopathy, or in amyloid plaques in white matter. One sensitive ... Aβ can also form the deposits that line cerebral blood vessels in cerebral amyloid angiopathy. The plaques are composed of a ... March 2020). "Prominent amyloid plaque pathology and cerebral amyloid angiopathy in APP V717I (London) carrier - phenotypic ... "The length of amyloid-beta in hereditary cerebral hemorrhage with amyloidosis, Dutch type. Implications for the role of amyloid ...
Candidate Biomarker for Immunotherapy in Alzheimer's Disease and Cerebral Amyloid Angiopathy". Frontiers in Neurology. 6: 207. ... "Spontaneous ARIA-like Events in Cerebral Amyloid Angiopathy-Related Inflammation: A Multicenter Prospective Longitudinal Cohort ... "Amyloid Related Imaging Abnormalities (ARIA) in Amyloid Modifying Therapeutic Trials: Recommendations from the Alzheimer's ... Amyloid-related imaging abnormalities (ARIA) are abnormal differences seen in magnetic resonance imaging of the brain in ...
Revesz T, Ghiso J, Lashley T, Plant G, Rostagno A, Frangione B, Holton JL (September 2003). "Cerebral amyloid angiopathies: a ... AII amyloid can be induced in mice by a variety of β-sheet rich amyloid fibrils, and cerebral tauopathy can be induced by brain ... Subsequent research has shown that many different proteins can form amyloid, and that all amyloids show birefringence in cross- ... Rudolf Virchow coined the term amyloid ("starch-like") to describe a substance in cerebral corpora amylacea that exhibited a ...
"Prominent amyloid plaque pathology and cerebral amyloid angiopathy in APP V717I (London) carrier - phenotypic variability in ... "Pathogenic effects of cerebral amyloid angiopathy mutations in the amyloid beta-protein precursor". Annals of the New York ... Mutations in critical regions of amyloid precursor protein, including the region that generates amyloid beta (Aβ), cause ... Zheng H, Koo EH (2006). "The amyloid precursor protein: beyond amyloid". Molecular Neurodegeneration. 1 (1): 5. doi:10.1186/ ...
Cerebral amyloid angiopathy is found in 90% of the cases at autopsy, with 25% being severe CAA. Cerebral microbleeds (CMB) ... Cerebral atherosclerosis is a type of atherosclerosis where build-up of plaque in the blood vessels of the brain occurs. Some ... The risk of cerebral atherosclerosis and its associated diseases appears to increase with increasing age; however there are ... Diseases cerebral atherosclerosis and associated diseases can cause are: Alzheimer's disease Alzheimer's disease is a form of ...
Subsequent media reports indicated that Sharon had been diagnosed with cerebral amyloid angiopathy (CAA) during his December ...
Her research program is investigating the glymphatic system is affected in cerebral amyloid angiopathy, Alzheimer's Disease, ...
... cerebral amyloid angiopathy. Valentina Cortese, 96, Italian actress (Malaya, Brother Sun, Sister Moon, Day for Night). Lutz ...
Bouton died at home on July 10, 2019, after weeks of hospice care for cerebral amyloid angiopathy, at age 80. Ball Four has ...
Cerebral amyloid angiopathy (CAA), a blood vessel failure often associated with Alzheimer's disease, utilizes dilated VRS to ... As such, VRS in the cerebral cortex may drain β-amyloid in interstitial fluid less effectively than VRS in the basal ganglia. ... In support of this hypothesis, studies have noted the greater frequency of β-amyloid plaques in the cerebral cortex than in the ... of hypointesities in susceptibility-weighted images to tissue histology in dementia patients with cerebral amyloid angiopathy: ...
... for the treatment of Alzheimer's disease and cerebral amyloid angiopathy. On December 22, 2021, Novartis announced that the US ... an Investigational RNAi Therapeutic for the Treatment of Alzheimer's Disease and Cerebral Amyloid Angiopathy". www.businesswire ... an investigational RNAi therapeutic targeting amyloid precursor protein (APP) ...
However, Aβ plaques (along with cerebral Aβ-amyloid angiopathy) can now be detected in the brains of living subjects. This is ... Amyloid plaques (also known as neuritic plaques, amyloid beta plaques or senile plaques) are extracellular deposits of the ... 2019). "Different aspects of Alzheimer's disease-related amyloid β-peptide pathology and their relationship to amyloid positron ... Amyloid beta (Aβ) is a small protein, most often 40 or 42 amino acids in length, that is released from a longer parent protein ...
Cerebral amyloid angiopathy (CAA) is a form of angiopathy in which amyloid beta peptide deposits in the walls of small to ... The aim in cerebral amyloid angiopathy is to treat the symptoms, as there is no current cure. Physical, occupational and/or ... Cerebral amyloid angiopathy can be presented with lobar intracerebral hemorrhage or microbleeds in the brain. The bleeding ... "Cerebral amyloid angiopathy: MedlinePlus Medical Encyclopedia". www.nlm.nih.gov. Retrieved 2015-05-27. "UpToDate". www.uptodate ...
... is a condition in which proteins called amyloid build up on the walls of the arteries in the brain. CAA causes bleeding into ... Cerebral amyloid angiopathy (CAA) is a condition in which proteins called amyloid build up on the walls of the arteries in the ... Emerging concepts in sporadic cerebral amyloid angiopathy. Brain. 2017;140(7):1829-1850. PMID: 28334869 pubmed.ncbi.nlm.nih.gov ... Greenberg SM, Charidimou A. Diagnosis of cerebral amyloid angiopathy: evolution of the Boston criteria. Stroke. 2018;49(2):491- ...
... of the cerebral cortex and the leptomeninges. It is a component of any disorder in which amyloid is deposited in the brain, and ... refers to the deposition of β-amyloid in the media and adventitia of small and mid-sized arteries (and, less frequently, veins ... The Boston Cerebral Amyloid Angiopathy Group has elaborated guidelines for the diagnosis of cerebral amyloid angiopathy (CAA) ... encoded search term (Cerebral Amyloid Angiopathy) and Cerebral Amyloid Angiopathy What to Read Next on Medscape ...
We postulated that cerebral amyloid angiopathy (CAA), characterised by cortical vascular amyloid deposits, is associated with ... Cortical atrophy in patients with cerebral amyloid angiopathy: a case-control study Lancet Neurol. 2016 Jul;15(8):811-819. doi ... Cerebral Amyloid Angiopathy / complications* * Cerebral Amyloid Angiopathy / diagnostic imaging* * Cerebral Amyloid Angiopathy ... Interpretation: The appearance of cortical thinning in patients with HCHWA-D indicates that vascular amyloid is an independent ...
Dementia in hereditary cerebral hemorrhage with amyloidosis-Dutch type is associated with cerebral amyloid angiopathy but is ...
Value of Magnetic Susceptibility-Weighted Imaging and Routine Magnetic Resonance Imaging in Cerebral Amyloid Angiopathy ... resonance imaging in cerebral amyloid angiopathy hemorrhage. A total of 64 patients with suspected cerebral amyloid angiopathy ... advantages in detecting the micro cerebral hemorrhage, and it can show the characteristics of the cerebral amyloid angiopathy ... Cerebral amyloid angiopathy (CAA) was a group of diseases characterized by the deposition of the insoluble fibrin (glycoprotein ...
Cerebral amyloid angiopathy with and without hemorrhage: Evidence for different disease phenotypes Academic Article ... OBJECTIVE: To gain insight into different cerebral amyloid angiopathy (CAA) phenotypes and mechanisms, we investigated cortical ...
Patient A.D., a physical fit senior woman, suffered a bleeding stroke, attributed to Cerebral Amyloid Angiopathy, in her left ...
Erratum: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy ... Erratum: Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy ...
The findings add to the body of evidence for use of antiplatelets in patients with cerebral amyloid angiopathy. ... Cerebral amyloid angiopathy is a disorder that affects the small blood vessels in the brain and causes them to be very leaky, ... Patients with cerebral amyloid angiopathy tend to be older. In these patients, there are also comorbidities such as high blood ... I think an interesting topic to study in the future would be to look at patients with cerebral amyloid angiopathy who also have ...
Off-label use of aducanumab for cerebral amyloid angiopathy. Lancet Neurol. 2021 08; 20(8):596-597. ...
The aim of the study is to identify clinical markers of vascular amyloiddeposition in patients with Alzheimers disease, focusing on cognitiveabilities and MRI features such as vascular reactivity.. ...
... a hereditary cerebral small vessel disease (SVD) characterized by the aggregation of the Notch3 extracellular domain. We found ... CAA is characterized by the aggregation of amyloid-β (Aβ) peptides and formation of Aβ deposits in the brain vasculature ... including a patient with hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D), and of AD cases without ... Cerebral amyloid angiopathy (CAA) is an age-related condition and a major cause of intracerebral hemorrhage and cognitive ...
... also known as congophilic angiopathy, is a recognized cause of lobar intracerebral haemorrhage in patients above the age of ... Cerebral amyloid angiopathy: incidence and complications in the aging brain. I. Cerebral hemorrhage. Stroke. 1983;14:915-23. ... Cerebral amyloid angiopathy (CAA), also known as congophilic angiopathy, is a recognized cause of lobar intracerebral ... Cerebral amyloid angiopathy (CAA), also known as congophilic angiopathy, is a recognized cause of lobar intracerebral ...
Cerebral microbleed distribution following cardiac surgery can mimic cerebral amyloid angiopathy. BMJ Neurology Open 2021;3: ...
CEREBRAL OEDEMA. Introduction. Cerebral amyloid angiopathy affects the small-to-medium-sized cerebral arteries most commonly ... Novel presenilin-1 mutation with widespread cortical amyloid deposition but limited cerebral amyloid angiopathy. Minoru Yasuda ... Association between apolipoprotein E e4 allele and arteriosclerosis, cerebral amyloid angiopathy, and cerebral white matter ... Transient focal leukoencephalopathy with cerebral oedema as a presentation of cerebral amyloid angiopathy ...
Stroke: A Journal of Cerebral Circulation Comparison of Boston Criteria v2.0/v1.5 for Cerebral Amyloid Angiopathy to Predict ... Comparison of the Boston Criteria v2.0/v1.5 for Cerebral Amyloid Angiopathy to Predict Recurrent Intracerebral Hemorrhage. ...
Objective: To investigate the association between the extent of cerebral amyloid angiopathy (CAA) and Apolipoprotein E (Apo E) ... PD-075 The Distribution of Cerebral Amyloid Angiopathy within the Brain with Alzheimers Disease May be Influenced by ...
... automated approach using interpretable neural networks to determine Alzheimers disease plaque and cerebral amyloid angiopathy ... Resulting network-derived amyloid beta (Aβ)-burden scores correlate well with established semi-quantitative scores on a 30-WSI ... We report a proof-of-concept deep learning pipeline that identifies specific neuropathologies-amyloid plaques and cerebral ... amyloid angiopathy-in immunohistochemically-stained archival slides. Using automated segmentation of stained objects and a ...
Cerebral amyloid angiopathy (CAA) is a devastating condition common in patients with Alzheimers disease but also observed in ... Border-associated macrophages promote cerebral amyloid angiopathy and cognitive impairment Border-associated macrophages ... promote cerebral amyloid angiopathy and cognitive impairment through vascular oxidative stress. Uekawa, Ken; Hattori, Yorito; ... Amyloid pathology and cognitive function were also examined. RESULTS:. The increase in blood flow evoked by whisker stimulation ...
Cerebral amyloid angiopathy (CAA). *Memory disorders. *Stroke. View All. Treats:. *Adult. View All. ...
APOE immunotherapy reduces cerebral amyloid angiopathy and amyloid plaques while improving cerebrovascular function. ... Dive into the research topics of APOE immunotherapy reduces cerebral amyloid angiopathy and amyloid plaques while improving ...
Magnetic resonance imaging (MRI) of cerebral microbleeds is the most reliable option for clinical diagnosis of suspected CAA. ... but it is thought to be the result of vessel weakening and rupture secondary to amyloid deposition. Little evidence has been ... Cerebral amyloid angiopathy (CAA) is an increasingly recognized cause of lobar intracerebral hemorrhage (ICH) and cognitive ... Rapidly Sequential and Fatal Hemorrhaging in a Case of Cerebral Amyloid Angiopathy Unusual clinical course, Challenging ...
Clinical considerations in early-onset cerebral amyloid angiopathy. June 06, 2023 *[ MEDLINE Abstract ] ... Amyloid-related imaging abnormalities (ARIA): radiological, biological and clinical characteristics. June 06, 2023 ... Somatic variants of MAP3K3 are sufficient to cause cerebral and spinal cord cavernous malformations. March 30, 2023 ... A data-driven study of Alzheimers disease related amyloid and tau pathology progression. July 11, 2023 ...
Ischemic changes related to cerebral small vessel disease and chronic hypoperfusion. *Evidence of cerebral amyloid angiopathy ... Anti-amyloid therapy-related brain and vascular changes. * ...
Cerebellar hemorrhages in patients with cerebral amyloid angiopathy. J Neurol Sci. 2019 Oct 15. 405:116418. [QxMD MEDLINE Link] ... Hemorrhage from tumors, blood dyscrasias, amyloid angiopathy, arteriovenous malformations, trauma, sympathomimetic abuse, and ... of obstructive hydrocephalus from ventricular compression may lead to increased intracranial pressure and decreased cerebral ...
On the Pathophysiology and Prevalence of Cerebral Amyloid Angiopathy. 529. Wassenberg, T. (2021). Monoamine neurotransmitter ... Amyloid-beta and amyloid associated proteins in the pathogenesis and diagnosis of Alzheimers Disease ... Temporal dynamics of cerebral small vessel disease. A motor perspective.. 550. Ausems, R (2022). First steps towards a pericyte ... Regulation of cerebral perfusion in Alzheimers disease: from seconds to months. 326. Güclü, U. (2018) Neural coding with deep ...
Cerebral amyloid angiopathy - With age, abnormal proteins including amyloid may deposit in the walls of arteries. These weaken ... Reversible cerebral vasoconstriction syndrome - Abnormal, excess squeezing of the walls of blood vessels in the head. ... Cerebral venous sinus thrombosis - Clot formation in the blood vessels draining blood away from the head. ...
  • Cerebral amyloid angiopathy (CAA) refers to the deposition of β-amyloid in the media and adventitia of small and mid-sized arteries (and, less frequently, veins) of the cerebral cortex and the leptomeninges. (medscape.com)
  • CAA was a cerebrovascular disease characterized by the deposition of β-amyloid protein in the media and adventitia of small and medium-sized vessels in the cerebral cortex, cortex, and pia mater. (ijpsonline.com)
  • Disorders of the brain microvasculature, collectively termed cerebral small vessel diseases (SVDs), are particularly common in the aging brain and encompass a variety of sporadic and hereditary conditions affecting small and medium-sized vessels in the cerebral cortex, subcortical white matter, and deep white matter [ 48 , 68 ]. (biomedcentral.com)
  • Coarse granular deposits of PrP in cerebral cortex, basal ganglia, and thalamus. (cdc.gov)
  • PrP microplaques, synaptic and granular accumulations of PrP restricted to cerebral cortex, basal ganglia, and thalamus. (cdc.gov)
  • These areas are the cerebral cortex, the hippocampus, the amygdala, several basal and thalamic nuclei, and the cerebellar cortical Purkinje cells. (vin.com)
  • Micrograph of a section of the cerebral cortex from a person with Alzheimer's disease , immunostained with an antibody to amyloid beta (brown), a protein fragment that accumulates in amyloid plaques and cerebral amyloid angiopathy . (wikipedia.org)
  • Micrograph of immunostained α-synuclein (brown) in Lewy bodies (large clumps) and Lewy neurites (thread-like structures) in the cerebral cortex of a patient with Lewy body disease , a synucleinopathy . (wikipedia.org)
  • Alzheimer Disease Alzheimer disease causes progressive cognitive deterioration and is characterized by beta-amyloid deposits and neurofibrillary tangles in the cerebral cortex and subcortical gray matter. (msdmanuals.com)
  • Cerebral amyloid angiopathy can be presented with lobar intracerebral hemorrhage or microbleeds in the brain. (wikipedia.org)
  • The Boston Cerebral Amyloid Angiopathy Group has elaborated guidelines for the diagnosis of cerebral amyloid angiopathy (CAA) associated with intracranial hemorrhage (ICH). (medscape.com)
  • Hereditary cerebral hemorrhage with amyloidosis-Dutch type is an autosomal-dominant disorder with complete penetrance. (medscape.com)
  • Hereditary cerebral hemorrhage with amyloidosis-Icelandic type is also autosomal dominant. (medscape.com)
  • Dementia in hereditary cerebral hemorrhage with amyloidosis-Dutch type is associated with cerebral amyloid angiopathy but is independent of plaques and neurofibrillary tangles. (alzforum.org)
  • To investigate the diagnostic value of the magnetic susceptibility-weighted imaging and routine magnetic resonance imaging in cerebral amyloid angiopathy hemorrhage. (ijpsonline.com)
  • A total of 64 patients with suspected cerebral amyloid angiopathy hemorrhage diagnosed in our hospital from January 2018 to January 2019 were included in the study. (ijpsonline.com)
  • The consistency of the two detection methods in the diagnosis of cerebral amyloid angiopathy hemorrhage and the difference in image quality were analyzed. (ijpsonline.com)
  • Magnetic susceptibility-weighted imaging has obvious advantages in detecting the micro cerebral hemorrhage, and it can show the characteristics of the cerebral amyloid angiopathy multiple hemorrhages, and its diagnostic value was better than that of routine routine magnetic resonance imaging. (ijpsonline.com)
  • The disease was clinically characterized by multiple and complex intracerebral hemorrhages, so it was also known as cerebral amyloid angiopathy hemorrhage (CAAH) [ 2 , 3 ]. (ijpsonline.com)
  • OBJECTIVE: To gain insight into different cerebral amyloid angiopathy (CAA) phenotypes and mechanisms, we investigated cortical superficial siderosis (CSS), a new imaging marker of the disease, and its relation with APOE genotype in patients with pathologically proven CAA, who presented with and without intracerebral hemorrhage (ICH). (mcmaster.ca)
  • Research conducted by Sheharyar Jamali, MD, and Michelle Lin, MD, MPH, showed that aspirin lowers the risk of ischemic stroke without increasing the risk of intracranial hemorrhage in patients with cerebral amyloid angiopathy. (neurologylive.com)
  • Cerebral amyloid angiopathy is a disorder that affects the small blood vessels in the brain and causes them to be very leaky, thus increasing the risk of intracranial hemorrhage. (neurologylive.com)
  • Cerebral amyloid angiopathy (CAA) is an age-related condition and a major cause of intracerebral hemorrhage and cognitive decline that shows close links with Alzheimer's disease (AD). (biomedcentral.com)
  • Here, applying an advanced protocol for the isolation of parenchymal microvessels from post-mortem brain tissue combined with liquid chromatography tandem mass spectrometry (LC-MS/MS), we determined the proteomes of CAA type 1 cases (n = 12) including a patient with hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D), and of AD cases without microvascular amyloid pathology (n = 13) in comparison to neurologically healthy controls (n = 12). (biomedcentral.com)
  • While mostly occurring as a sporadic condition, CAA can also develop from rare APP mutations such as the E693Q mutation, which causes hereditary cerebral hemorrhage with amyloidosis-Dutch type (HCHWA-D) [ 33 ]. (biomedcentral.com)
  • Since CAA can be caused by the same amyloid protein that is associated with Alzheimer's dementia, brain bleeds are more common in people who have a diagnosis of Alzheimer's disease. (wikipedia.org)
  • We postulated that cerebral amyloid angiopathy (CAA), characterised by cortical vascular amyloid deposits, is associated with cortical tissue loss independent of parenchymal Alzheimer's disease pathology. (nih.gov)
  • We tested this hypothesis in patients with hereditary cerebral haemorrhage with amyloidosis-Dutch type (HCHWA-D), a monogenetic disease with minimal or no concomitant Alzheimer's disease pathology, as well as in patients with sporadic CAA and healthy and Alzheimer's disease controls. (nih.gov)
  • Objective: To investigate the association between the extent of cerebral amyloid angiopathy (CAA) and Apolipoprotein E (Apo E) e4 allele in Alzheimer's disease (AD). (confex.com)
  • Cerebral amyloid angiopathy (CAA) is a devastating condition common in patients with Alzheimer's disease but also observed in the general population . (bvsalud.org)
  • CAA-ri has gained additional interest for its notable similarities to amyloid-related imaging abnormalities, a complication of immunotherapy treatments in Alzheimer's disease patients. (iospress.com)
  • Appropriate use criteria for amyloid PET: a report of the amyloid imaging task force, the Society of Nuclear Medicine and Molecular Imaging, and the Alzheimer's Association. (intramed.net)
  • Isolation of low-molecular-weight proteins from amyloid plaque fibers in Alzheimer's disease. (intramed.net)
  • [9] However, some proteinaceous lesions lack birefringence and contain few or no classical amyloid fibrils, such as the diffuse deposits of amyloid beta (Aβ) protein in the brains of people with Alzheimer's. (wikipedia.org)
  • Recent research also suggested that anti-amyloid therapies for Alzheimer's disease accelerated brain atrophy , a point raised at the advisory committee meeting by panelist Tanya Simuni, MD, of Northwestern University in Chicago. (medpagetoday.com)
  • The search to find therapeutic targets in Alzheimer's disease (AD) has been dominated for over 25 years by research into the roles in the initiation and progression of dementia of the amyloid beta protein (Aβ) [1, 2], derived from the β-pathway of amyloid beta protein (AβPP) cleavage. (j-alz.com)
  • Emerging concepts in sporadic cerebral amyloid angiopathy. (medlineplus.gov)
  • Deposited amyloid protein in these patients is identical to the amyloid protein seen in sporadic cases, and the likely genetic defect is in the amyloid protein precursor protein ( APP ) gene on chromosome 21. (medscape.com)
  • Review: sporadic cerebral amyloid angiopathy. (intramed.net)
  • The findings add to the body of evidence for use of antiplatelets in patients with cerebral amyloid angiopathy. (neurologylive.com)
  • Jamali, a neurologist from Mayo Clinic, noted that despite the insignificance, these results open the door for future research opportunities to evaluate the use of antiplatelets among patients with cerebral amyloid angiopathy and other similar diseases. (neurologylive.com)
  • Patients with cerebral amyloid angiopathy tend to be older. (neurologylive.com)
  • How do we prevent the ischemic stroke burden in these patients with cerebral amyloid angiopathy? (neurologylive.com)
  • The best study we can do is a randomized controlled trial, where we randomize patients with cerebral amyloid angiopathy into an aspirin versus no aspirin arm and see whether there's an increased risk of ischemic or hemorrhagic stroke in that scenario. (neurologylive.com)
  • I think an interesting topic to study in the future would be to look at patients with cerebral amyloid angiopathy who also have another disorder called atrial fibrillation. (neurologylive.com)
  • The proteomic profile of CAA type 1 was characterized by massive enrichment of multiple predominantly secreted proteins and showed significant overlap with the recently reported brain microvascular proteome of patients with cerebral autosomal-dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL), a hereditary cerebral small vessel disease (SVD) characterized by the aggregation of the Notch3 extracellular domain. (biomedcentral.com)
  • We report a biomarker and genetic evaluation of four patients with cerebral amyloid angiopathy-related inflammation (CAA-ri) treated with corticosteroids. (iospress.com)
  • The vascular amyloid pathology characteristic of CAA can be classified as either Type 1 or Type 2, the latter type being the more common. (wikipedia.org)
  • Type 1 CAA pathology entails detectable amyloid deposits within cortical capillaries as well as within the leptomeningeal and cortical arteries and arterioles. (wikipedia.org)
  • In type 2 CAA pathology, amyloid deposits are present in leptomeningeal and cortical arteries and arterioles, but not in capillaries. (wikipedia.org)
  • Amyloid pathology and cognitive function were also examined. (bvsalud.org)
  • This approach has never been fully accepted by the AD research community [6-12] and epidemiological population based studies of ageing consistently find complex relationships between age, amyloid pathology, in-life factors such as education, and dementia status [13-17]. (j-alz.com)
  • a physiological measure of vascular dysfunction) were analysed to understand the potential mechanistic link between vascular amyloid and cortical thickness. (nih.gov)
  • The appearance of cortical thinning in patients with HCHWA-D indicates that vascular amyloid is an independent contributor to cortical atrophy. (nih.gov)
  • 2 The plaque is then deposited within the cerebral vasculature, primarily the leptomeningeal and cortical vessels. (touchneurology.com)
  • Cerebral microbleeds (CMBs) are frequently found in the healthy elderly. (dovepress.com)
  • The prevalence of cerebral microbleeds is similar to other countries. (dovepress.com)
  • Cerebral microbleeds (CMBs) are 2-10mm, rounded or circular, well-defined hypointense lesions on gradient-echo T2*-weighted images (GRE T2*WI) or susceptibility-weighted images (SWI) of magnetic resonance imaging (MRI). (dovepress.com)
  • In all cases, it is defined by the deposition of amyloid beta (Aβ) in the leptomeningeal and cerebral vessel walls. (wikipedia.org)
  • Mutations in the amyloid precursor protein (APP), Presenilin (PS) 1 and PS2 genes can result in increased rates of cleavage of the APP into Aβ. (wikipedia.org)
  • People with CAA have deposits of amyloid protein in the walls of blood vessels in the brain. (medlineplus.gov)
  • CAA is characterized by the misfolding and excessive vascular deposition of amyloid-β (Aβ) peptides, which are generated by multiple proteolytical processing of the β-amyloid precursor protein (APP) [ 60 ]. (biomedcentral.com)
  • Beta-amyloid plaque is formed by the degradation of amyloid precursor protein via secretases. (touchneurology.com)
  • In 1859, Friedreich and Kekulé demonstrated that, rather than consisting of cellulose, "amyloid" actually is rich in protein. (wikipedia.org)
  • 1 As one feature of cerebral small vessel disease (CSVD), CMBs were found to have a close association with ischemic or hemorrhagic stroke, dementia, or even mortality. (dovepress.com)
  • Vascular cognitive impairment and dementia is acute or chronic cognitive deterioration due to diffuse or focal cerebral infarction that is most often related to cerebrovascular disease. (msdmanuals.com)
  • Amyloid fibrils may deposit in cerebral vessels, as in β-amyloid CAA, or form senile plaques in brain parenchyma. (medscape.com)
  • We report a proof-of-concept deep learning pipeline that identifies specific neuropathologies-amyloid plaques and cerebral amyloid angiopathy-in immunohistochemically-stained archival slides. (nature.com)
  • Border-associated macrophages promote cerebral amyloid angiopathy and cognitive impairment through vascular oxidative stress. (bvsalud.org)
  • Could Blood Transfusions Transmit Vascular Amyloid? (alzforum.org)
  • Because cerebral amyloid angiopathy is a main cause of such bleeds, the findings imply that aggregated amyloid in the donor's blood could potentially seed vascular deposits in the recipient, the authors argued. (alzforum.org)
  • Greenberg SM, Charidimou A. Diagnosis of cerebral amyloid angiopathy: evolution of the Boston criteria. (medlineplus.gov)
  • His initial diagnosis was cerebral vasculitis based on computed tomography displaying bilateral vasogenic oedema, a 4 mm midline shift and a right thalamic lacunar infarct. (touchneurology.com)
  • He was subsequently hospitalized at a rural hospital with an initial diagnosis of cerebral vasculitis based on computed tomography (CT) imaging showing bilateral vasogenic oedema, a 4 mm midline shift and a right thalamic lacunar infarct. (touchneurology.com)
  • Cerebral amyloid angiopathy (CAA), also known as congophilic angiopathy, is a recognized cause of lobar intracerebral haemorrhage in patients above the age of 50 years. (touchneurology.com)
  • Mark's presentation was on The Edinburgh CT and genetic criteria for lobar intracerebral haemorrhage associated with cerebral amyloid angiopathy. (ed.ac.uk)
  • Cerebral amyloid angiopathy (CAA) is a condition in which proteins called amyloid build up on the walls of the arteries in the brain. (medlineplus.gov)
  • Cerebral amyloid angiopathy - With age, abnormal proteins including amyloid may deposit in the walls of arteries. (tuftsmedicalcenter.org)
  • [9] Subsequent research has shown that many different proteins can form amyloid, and that all amyloids show birefringence in cross- polarized light after staining with the dye Congo red , as well as a fibrillar ultrastructure when viewed with an electron microscope . (wikipedia.org)
  • 1 It is known to be due to deposition of a variant of amyloid (beta-amyloid plaque) in cerebral blood vessels. (touchneurology.com)
  • Impaired elimination and accumulation of soluble and insoluble β-amyloid peptide may underlie the pathogenesis of CAA and explain the link between CAA and Alzheimer disease (AD). (medscape.com)
  • Amyloid-dependent and amyloid-independent stages of Alzheimer disease. (intramed.net)
  • Down syndrome, Alzheimer disease, and cerebral amyloid angiopathy: the complex triangle of brain amyloidosis. (bvsalud.org)
  • Cerebrovascular amyloid deposits can be observed in both large (e.g. leptomeningeal) vessels and small parenchymal arterioles and capillaries, with their presence in capillaries determining the classification of CAA into two subtypes. (biomedcentral.com)
  • Cerebral Amyloid Angiopathy-Related Inflammation Biomarkers: Where are we Now? (iospress.com)
  • Soluble ACE2 in the brain correlated inversely with cognitive function scores, pericyte markers [PDGFRβ (platelet-derived growth factor receptor β) and aminopeptidase N (ANPEP)], and the caveolin1 marker, but correlated positively with insoluble phosphor-tau (S396/404 epitope) and soluble amyloid-β peptides (Aβ) levels. (news-medical.net)
  • This case highlights unique imaging findings of cerebral amyloid angiopathy-related inflammation (CAA-ri). (touchneurology.com)
  • Cerebral amyloid angiopathy- related inflammation (CAA-ri) is an aggressive disease subtype of CAA with characteristic clinical and radiological findings. (iospress.com)
  • CAA is characterized by the aggregation of amyloid-β (Aβ) peptides and formation of Aβ deposits in the brain vasculature resulting in a disruption of the angioarchitecture. (biomedcentral.com)
  • The transportation of these fuel molecules requires sufficient blood flow through a cerebral vasculature with adequate capacity. (vin.com)
  • Patient A.D., a physical fit senior woman, suffered a bleeding stroke, attributed to Cerebral Amyloid Angiopathy, in her left occipital lobe. (amyloidangiopathy.com)
  • What motivated me to do this project was seeing patients in the hospital with cerebral amyloid antipathy who presented with ischemic stroke. (neurologylive.com)
  • Ischemic Stroke Ischemic stroke is sudden neurologic deficits that result from focal cerebral ischemia associated with permanent brain infarction (eg, positive results on diffusion-weighted MRI). (msdmanuals.com)
  • However, there are types involving other amyloid peptides: the "Icelandic type" is associated with Cystatin C amyloid (ACys). (wikipedia.org)
  • The amyloid material is only found in the brain and as such the disease is not related to other forms of amyloidosis. (wikipedia.org)
  • Familial amyloidosis-Finnish type is associated with gelsolin amyloid (AGel). (wikipedia.org)
  • [ 1 ] It is a component of any disorder in which amyloid is deposited in the brain, and it is not associated with systemic amyloidosis. (medscape.com)
  • The relatively rapid appearance of ICH in recipients is inconsistent with seeded cerebral β-amyloidosis, which generally takes many years or decades to reveal itself in humans," Walker wrote. (alzforum.org)
  • apolipoprotein E (APOE) ε2 and ε4 are associated with increased risk of getting cerebral amyloid antipathy. (wikipedia.org)
  • What is the current state of research for cerebral amyloid antipathy? (neurologylive.com)
  • The term congophilic is sometimes used because the presence of the abnormal aggregations of amyloid can be demonstrated by microscopic examination of brain tissue after staining with Congo red. (wikipedia.org)
  • However, some evidence suggests that the amyloid is produced in the smooth muscle cells of the tunica media as a response to damage to the vessel wall (perhaps by arteriosclerosis or hypertension). (medscape.com)
  • Its mechanism is unknown but probably relates to altered permeability of cerebral blood vessels that results from endothelial dysfunction secondary to β-amyloid accumulation in the vessel wall. (bmj.com)
  • MRI was performed at 3Tesla and cardiovascular risk factors (eg, age, smoking history, and hypertension), cerebral small vessel disease (CSVD) markers (eg, white matter hyperintensities, lacunar infarction, and enlarged perivascular space) and genetic information (eg, APOE, CR1) were recorded. (dovepress.com)
  • Many studies suggested that deep CMBs may relate to hypertensive small vessel disease (HTN-SVD) and strictly lobar CMBs for cerebral amyloid angiopathy (CAA), 1 but the risk factors of CMBs are not entirely clear. (dovepress.com)
  • Adverse events included amyloid-related imaging abnormalities (ARIA) with edema or effusions (ARIA-E), which occurred in 13% of people who received lecanemab. (medpagetoday.com)
  • I believe this collaboration will lead to important breakthroughs in understanding brain clearance and reveal key insights as to why cerebral amyloid angiopathy and other dementias occur, and how we can treat and prevent them. (uri.edu)
  • Magnetic resonance imaging (MRI) showed diffuse vasogenic oedema in both cerebral hemispheres, intervening zones of gyral oedema, a tiny acute petechial haemorrhage and leptomeningeal enhancement with diffuse signal dropout supportive of amyloid angiopathy ( Figure 1A ). (touchneurology.com)
  • The dynamic between accumulation and clearance of amyloid may be related to impaired drainage from perivascular basement membranes. (medscape.com)
  • T2 gradient echo (GRE) findings included innumerable findings of signal dropout scattered throughout the right and left cerebral hemispheres peripherally at zones of grey-white matter differentiation. (touchneurology.com)
  • The consortium will work with innovative transgenic and gene-edited rodent models developed by Van Nostrand, who has studied cerebral amyloid angiopathy for nearly 30 years and recently co-authored key findings on the role of brain clearance in the disorder with investigators at Yale University. (uri.edu)
  • The overarching consortium aims are to establish a data-driven, integrated multi-scale understanding of perivascular brain clearance in health and cerebral amyloid angiopathy, translate experimental findings from rodent models to the human brain, and identify relevant driving forces to be tested in future clinical trials to enhance brain clearance. (uri.edu)
  • Cerebral amyloid angiopathy (CAA) was a group of diseases characterized by the deposition of the insoluble fibrin (glycoprotein) in brain tissue. (ijpsonline.com)
  • 5 Any diseases which affect the cerebral blood vessels will cause disturbances of the cerebral blood flow (CBF) which in turn can lead to tissue damage. (vin.com)
  • Cerebral amyloid angiopathy (CAA) is a form of angiopathy in which amyloid beta peptide deposits in the walls of small to medium blood vessels of the central nervous system and meninges. (wikipedia.org)
  • Initially, the amyloid-beta plaque is deposited in the tunica media and adventitia of blood vessels and impairs smooth muscle cells, 3 leading to fibrinoid necrosis. (touchneurology.com)
  • Reversible cerebral vasoconstriction syndrome - Abnormal, excess squeezing of the walls of blood vessels in the head. (tuftsmedicalcenter.org)
  • Cerebral venous sinus thrombosis - Clot formation in the blood vessels draining blood away from the head. (tuftsmedicalcenter.org)
  • Evidence suggests that while P3-40 is seen in the soluble compartment, P3-42 is not [19], though it has been detected neuropathologically in fleecy amyloid deposits [22]. (j-alz.com)
  • In a 6-0 vote, the agency's Peripheral and Central Nervous System Drugs Advisory Committee fully backed the evidence supporting the anti-amyloid monoclonal antibody. (medpagetoday.com)