Expression of somatostatin in the brain declines during aging in various mammals including apes and humans. 4 key findings →
Evidence: low
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27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Expression of somatostatin in the brain declines during aging in various mammals including apes and humans. 4 key findings →
Evidence: low
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Patients with Alzheimer disease have reduced levels of sRAGE in plasma compared with patients with vascular dementia and controls. 2 key findings →
Design: cross-sectional Participants: 152 Evidence: low
Full summary, score breakdown and related studies → Original source
A reasonably accurate, validated model has been produced, with clinical application through a scored point system, to assist clinicians, residents, and family members in defining good goals of care around end-of-life care. 1 key finding →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Future longitudinal studies with trauma control subjects and neuropsychological measures are indicated to further elucidate the relationship between hippocampus and behavioral abnormalities in young PTSD subjects. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Fish consumption may be associated with slower cognitive decline with age. 5 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Multivariate analyses assessed the strength of association of comorbid conditions with epilepsy as compared with the general population. 3 key findings →
Participants: 49,000 Evidence: low
Full summary, score breakdown and related studies → Original source
We assessed cerebrospinal fluid (CSF) levels of tau and other biomarkers of neurodegenerative disease. 4 key findings →
Participants: 64 Evidence: low
Full summary, score breakdown and related studies → Original source
M ILD COGNITIVE i m p a i r m e n t (MCI) has been actively investigated for the past decade. , 2 The term was coined in the late 1980s by the New York University group to identify individuals who were not cognitively normal for age and yet did not have overt dementia, and their outcomes were described in an article examining predictors of dementia by Flicker et al in the early 1990s. Flicker et al characterized MCI as equivalent to a Global Deterioration Scale rating of 3 and found that a diagnostic approach combining a careful, structured interview and the appropriate neuropsychological tests can discriminate those individuals with MCI likely to experience cognitive deterioration from those with a benign prognosis. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
In the Cardiovascular Health Cognition Study, consumption of fatty fish was associated with a reduced risk of dementia and Alzheimer disease for those without the APOE epsilon4 allele. 2 key findings →
Evidence: low
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APOE genotype strongly predicts the rate of cognitive decline in Alzheimer disease. 1 key finding →
Participants: 218 Evidence: low
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Inflammation has been implicated as a pathogenetic factor in Alzheimer disease, possibly via effects on beta-amyloid (Abeta). 1 key finding →
Evidence: high
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Dementia is one of the major causes of dependency after stroke. 3 key findings →
Evidence: low
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Our findings suggest that the onset of dementia-related syndromes may be initiated by repetitive cerebral concussions in professional football players. 5 key findings →
Evidence: low
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Dementia-associated weight loss begins before the onset of the clinical syndrome and accelerates by the time of diagnosis. 4 key findings →
Evidence: low
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Alzheimer disease (AD) and, to a lesser extent, dementia with Lewy bodies (DLB) showed more pronounced MTA. 3 key findings →
Participants: 39 Evidence: low
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Like acetylcholinesterase, butyrylcholinesterase (BChE) inactivates the neurotransmitter acetylcholine (ACh) and is hence a viable therapeutic target in Alzheimer's disease, which is characterized by a cholinergic deficit. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer disease, increased beta-secretase (BACE1) activity has been associated with neurodegeneration and accumulation of amyloid precursor protein (APP) products. 3 key findings →
Evidence: low
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Accumulating evidence suggests that neurodegeneration induced by pathogenic proteins depends on contributions from surrounding glia. 4 key findings →
Evidence: low
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The results suggest that brain response differences are not due to poorer general memory abilities, differential atrophy, or brain response during control conditions, but instead appear to be directly influenced by APOE genotype. 4 key findings →
Evidence: low
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The APOE*E4 genotype status appears to have a greater deleterious effect on gross hippocampal pathology and memory performance in women than in men. 4 key findings →
Participants: 193 Evidence: low
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Alzheimer's disease (AD) is the most common form of neurodegenerative dementia and affects up to 15 million people worldwide. 3 key findings →
Evidence: low
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The authors assessed whether measures of hippocampal water diffusivity at baseline can predict future progression to Alzheimer disease (AD) in amnestic mild cognitive impairment (aMCI). 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood pressure and indicators of small-vessel disease in the brain may be associated with atrophy of structures affected by Alzheimer pathology. 4 key findings →
Evidence: low
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In nondemented individuals, entorhinal cortex atrophy is associated with risk of Alzheimer disease. 3 key findings →
Participants: 58 Evidence: low
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Beta-secretase (BACE1) is the rate-limiting protease for the generation of the amyloid beta-peptide (Abeta) in Alzheimer disease. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Free full text links and the Full text may need a subscription label come from Unpaywall, Europe PMC and OpenAlex records of free copies, checked 10 Oct 2026. A study with neither is unknown, not paywalled. Show only studies that are free to read
This is alzhub's own score. It is not an official metric, not an impact factor, and no journal, publisher or ranking body endorses it. We built it so that a reader who is not a scientist can tell a landmark trial from a conference abstract without having to already know the difference. Every point comes from one of 20 components, all of them printed on the study itself, so you can disagree with our arithmetic rather than having to trust the total.
Journals are placed in ordered tiers, never given a numeric impact factor — we could not verify current impact factors from a source we control, and an invented one would be worse than none. Tier 1 is the top-tier general journals (NEJM, The Lancet, JAMA, Nature, Science, Nature Medicine); tier 2 is the leading specialty journals; tier 3 is every other peer-reviewed journal. A separate part scores how much the journal's own papers are cited, which tells the tier-3 journals apart.
Two rules we don't bend. First, we never fill in a missing value: if a record does not state a sample size or a design, that component scores zero, and if we simply have no data for a part, such as a citation count, that part is left out and the study is scored on the parts we could check. The study card says which. Second, anything that is not a peer-reviewed article is capped at 16/100 and carries a warning chip — so a conference abstract or a company press release can never outrank a peer-reviewed paper, no matter how good it looks.
We rank a rigorous null result — a good trial showing that something does not work — above an early positive finding. Someone deciding whether to buy a supplement is served by that, and the rigour is already counted by the design and journal components.
The score is computed from the published data alone and is reproducible: the same file always yields the same numbers.
See the whole rubric drawn out → — four charts covering all 27,380 studies: how the scores are spread and where the cap bites, which of the 20 components the library is strong and weak on, which subjects rest on stronger evidence, and what kinds of study each subject is actually built from.
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), plus smaller pulls from PubMed, Crossref and medRxiv. If a study, a drug, or a finding isn't here, that is not evidence it doesn't exist in the literature — it may simply not have been pulled in yet.
1,032 records (3.8% of the library) are not peer-reviewed — 962 of those are preprints posted before any journal review, and the rest are conference abstracts, regulatory notices and reports. Every study card on this page states its status plainly, and the score above is capped for anything that isn't a peer-reviewed article.
See the full, machine-readable breakdown of this library's coverage →