Microglia are the principal immune cells of the brain. 4 key findings →
Evidence: low
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28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Microglia are the principal immune cells of the brain. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Full text may need a subscription
Among 2157 older adults without dementia (mean [SD] age 71.2 [9.2] years; 1337 female [62.0%]), 1680 participants had longitudinal cognition data and 569 participants (26.4%) had APOE34/44 genotypes. 5 key findings →
Design: cohort study Participants: 1,680 Evidence: moderate
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In the first of five phases in the evolution of beta-amyloidosis Abeta deposits are found exclusively in the neocortex. 5 key findings →
Design: clinical trial Evidence: low
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Overall, the available evidence suggests that natural compounds confer multitarget neuroprotective effects that directly engage with key pathological mechanisms underlying AD. 4 key findings →
Design: systematic review Participants: 41 Evidence: high
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The study reported the cloning of a novel gene (E5-1) encoded on chromosome 1 with sequence similarity to the S182 gene on chromosome 14q24.3. 5 key findings →
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Slow paced breathing via heart rate variability (HRV) biofeedback stimulates vagus-nerve pathways that counter noradrenergic stress and arousal pathways that can influence production and clearance of Alzheimer's disease (AD)-related proteins. 2 key findings →
Participants: 108 Evidence: high
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Serum Abeta40/42 ratio was significantly higher in MDD patients than in controls, and this difference was seen for both elderly and young subjects. 5 key findings →
Design: cohort study Participants: 60 Evidence: moderate
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These findings suggest that DPP-4i use is associated with low amyloid burden and favorable long-term cognitive outcome in diabetic patients with ADCI. 2 key findings →
Design: longitudinal study Participants: 70 Evidence: moderate
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Apolipoprotein E is immunochemically localized to the senile plaques, vascular amyloid, and neurofibrillary tangles of Alzheimer disease. 2 key findings →
Evidence: low
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The association between the apoE epsilon4 allele and Alzheimer disease does not seem to be mediated by vascular factors. 1 key finding →
Participants: 1,449 Evidence: low
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Although Aβ did not differ by sex, cognitive decline was greater in females with higher Aβ. 3 key findings →
Participants: 755 Evidence: low
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The presence of epsilon 4 was associated with risk of developing AD on follow-up (relative risk, 1.92; 95% confidence interval, 1.27-2.89). 3 key findings →
Design: cohort study Participants: 624 Evidence: moderate
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Although there were no significant differences among the 3 groups of participants in their clinical ratings, neuropsychological test scores, hippocampal volumes (P = .60), or hippocampal glucose metabolism measurements (P = .12), there were significant group differences in their posterior cingulate glucose metabolism measurements (P = .001). 2 key findings →
Design: cross-sectional Participants: 31 Evidence: low
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Targeted sequencing of confirmed GWAS loci revealed an excess burden of deleterious coding mutations in LOAD, with the greatest burden observed in ABCA7 and BIN1. 4 key findings →
Participants: 176 Evidence: low
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The impact of APOE4 on brain metabolism and structure is modified by sex. 3 key findings →
Design: cross-sectional Participants: 274 Evidence: low
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Compared with individuals with the APOEepsilon3/epsilon3, the odds of having AD were significantly increased among those with 1 or more copies of the epsilon4 allele; the odds ratio (OR) for the epsilon3/epsilon4 genotype was 2.6 (95% confidence interval [CI], 1.8-3.7), and the OR for the epsilon4/epsilon4 genotype was 10.5 (95% CI, 5.1-21.8). 3 key findings →
Design: case-control study Participants: 338 Evidence: moderate
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Phenotypic personality dimensions, primarily neuroticism and extraversion, moderate the relationship between APOE [Latin Small Letter Open E]-4 genotype and cognitive outcomes among older adults. 1 key finding →
Evidence: high
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The risk of dementia and Alzheimer's disease (AD) probably results from an interaction between genetic and environmental factors. 3 key findings →
Participants: 1,449 Evidence: low
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Plasma A beta levels are affected by age and by systemic and CNS vascular risk factors. 4 key findings →
Design: cross-sectional Participants: 55 Evidence: moderate
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We examined longitudinal associations between the apolipoprotein E ε4 allele (ApoE4(+) status) and several cognitive outcomes and tested effect modification by sex. 3 key findings →
Design: longitudinal study Participants: 113 Evidence: moderate
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This study confirms the association between genetic variants in SORL1 and AD. 5 key findings →
Design: case-control study Participants: 296 Evidence: moderate
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The APOE ε4 genetic variant is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) and is increasingly being implicated in other neurodegenerative diseases. 3 key findings →
Evidence: low
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10 of the 1,383 studies in this tag, 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.
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →