Each study has a usefulness score out of 100 (rubric version 4.0). Tap a score to see what makes it up.
Highest usefulness score first. Studies without a score come last.
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We evaluated the allele (and genotype frequencies in 60 Down syndrome (DS), 25 mothers and 57 controls from Sicily and its relation with mental retardation.
Why it matters
In 60 people with Down syndrome from Sicily, this study found the apolipoprotein E ε4 allele was less frequent than in controls and had no influence on the grade of mental retardation. The authors conclude that the role of Apo-E4 in Alzheimer disease cannot be extrapolated to dementia in Down syndrome.
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In just under 20 years the kynurenine family of compounds has developed from a group of obscure metabolites of the essential amino acid tryptophan into a source of intensive research, with postulated roles for quinolinic acid in neurodegenerative disorders, most especially the AIDS-dementia complex and Huntington's disease.
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Mechanisms by which astrocytes are irreversibly injured from ischemic brain injury remain incompletely defined.
Why it matters
This is an in vitro organ culture study of astrocytic clasmatodendrosis, a process described by Alzheimer over 90 years ago after reduced blood flow. It is a laboratory model and does not test any treatment, cure or prevention for Alzheimer's disease.
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Human immunodeficiency virus (HIV) infection selectively targets the striatum, a region rich in opioid receptor-expressing neural cells, resulting in gliosis and neuronal losses.
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Most biological findings in posttraumatic stress disorder (PTSD) are compatible with those of the chronic stress response, such as increased corticotropin-releasing factor (CRF) concentrations, catecholamine depletion within the central nervous system, and reduced hippocampal volume.
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The Maillard reaction that leads to the formation of advanced glycation end-products (AGEs) plays an important role in the pathogenesis of angiopathy in diabetic patients and in aging.
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Exonic and intronic mutations in Tau cause neurodegenerative syndromes characterized by frontotemporal dementia and filamentous tau protein deposits.
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An extensive literature stretching back decades has shown that prolonged stress or prolonged exposure to glucocorticoids-the adrenal steroids secreted during stress-can have adverse effects on the rodent hippocampus.
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36/100
A number of studies indicate that prolonged, major depression is associated with a selective loss of hippocampal volume that persists long after the depression has resolved.
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36/100
Age and estrogen treatment influenced fiber outgrowth and compensatory neuronal sprouting after unilateral entorhinal cortex lesions (ECL) which model Alzheimer disease-like deafferentation in the dentate gyrus of the hippocampus.
Why it matters
In female rats, age and estrogen affected compensatory sprouting after entorhinal cortex lesions, and estrogen's effect on GFAP mRNA differed between young and middle-aged animals. This is an animal study modeling Alzheimer-like deafferentation and does not establish any treatment for Alzheimer disease in people.
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We investigated by immunohistochemistry the deposition of alpha-synuclein in the brains of deceased patients with the parkinsonism-dementia complex (PDC) of Guam.
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36/100
Using quantitative structural MRI protocols, we examined the effects of age on alterations in entorhinal cortex (EC) volume.
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36/100
Mutations in Notch3 cause CADASIL (cerebral autosomal dominant adult onset arteriopathy), which leads to stroke and dementia in humans.
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36/100
Breakdown of cellular membranes is a characteristic feature of neuronal degeneration in acute (stroke) and chronic (senile dementia) neurological disorders.
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In 3 mature female horses of varying breeds, episodes of colic and depression for 14 days preceded an encephalopathic disorder with maniacal behaviour, anxiety, profuse sweating and, in one case, terminal opisthotonus.
Why it matters
This report describes three horses with high blood ammonia and a type of astrocyte change in the brain that shares a name with a finding seen in liver-related brain disease in people. It concerns horses with encephalopathy and does not test any treatment, prevention or cause of Alzheimer disease in humans.
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These findings require further work to determine if the abnormalities are an expression of the genetic liability to schizophrenia.
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N-methyl-D-aspartate (NMDA) receptor antagonists have therapeutic potential in numerous CNS disorders ranging from acute neurodegeneration (e.g. stroke and trauma), chronic neurodegeneration (e.g. Parkinson's disease, Alzheimer's disease, Huntington's disease, ALS) to symptomatic treatment (e.g. epilepsy, Parkinson's disease, drug dependence, depression, anxiety and chronic pain).
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The microtubule-associated protein tau regulates the dynamic stability of the neuronal cytoskeleton by interacting with microtubules.
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These data suggest that the overwhelming stress of maltreatment experiences in childhood is associated with adverse brain development.
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Receptor for advanced glycation end products (RAGE) is a member of the immunoglobulin superfamily of cell surface molecules and engages diverse ligands relevant to distinct pathological processes.
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In order to study the neurobiological basis of seasonal changes in hippocampal structure and function, the rate of cell proliferation was examined in male and female wild meadow voles captured during different seasons.
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Several clinical trials have evaluated the potential of antiglutamate drugs to improve outcome following acute ischaemic stroke, but to date, the results of these have been disappointing.
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We report a Japanese family with early onset hereditary frontotemporal dementia and a novel missense mutation (Ser305Asn) in the tau gene.
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Thyroid hormone abnormalities are strongly associated with Down Syndrome (DS) with elevated thyroid stimulating hormone (TSH) levels as the most consistent finding.
Why it matters
This study found elevated levels of the TSH-receptor protein in brain regions of people with Down syndrome and, unexpectedly, Alzheimer's disease. The finding was not specific to Down syndrome and the authors suggest it may reflect apoptosis, so it does not provide a treatment or prevention approach.
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36/100
The presenilin-1 (PS1) gene mutation (Pro117Leu), recently identified in a Polish family is characterized by the earliest reported onset (from 24-31 years) of Alzheimer disease (AD) and a very short duration of disease (4-6 years).
Why it matters
This study describes a presenilin-1 mutation associated with very early onset Alzheimer's disease and compares amyloid deposition in those patients to Down syndrome and sporadic Alzheimer's patients. It characterizes the effect of this mutation on amyloid buildup but does not test any treatment or prevention.
From across this topic
10 of the 4,748 studies in this topic, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Increased amyloid beta-peptide deposition in cerebral cortex as a consequence of apolipoprotein E genotype in late-onset Alzheimer disease
- Cytokines and cognition--the case for a head-to-toe inflammatory paradigm
- Black raspberry supplementation on overweight and Helicobacter pylori infected mild dementia patients a pilot study
- ApoE4 markedly exacerbates tau-mediated neurodegeneration in a mouse model of tauopathy
- Repetitive injury induces phenotypes associated with Alzheimer’s disease by reactivating HSV-1 in a human brain tissue model
- Possible association between PM2.5 and neurodegenerative diseases: A systematic review
- MAPT mutations, tauopathy, and mechanisms of neurodegeneration
- Molecular pathology and synaptic loss in primary tauopathies: an 18F-AV-1451 and 11C-UCB-J PET study
- Amygdala and hippocampal volumes in familial early onset major depressive disorder
- Novel fully human high-affinity anti-TREM2 antibody shows efficacy in clinically relevant Alzheimer´s mouse model