27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 1583 articles, data subjected from the 24 studies (including 3562 patients who experienced delirium and 6987 controls who did not) were included in a random-effects meta-analysis for pooled effect estimates and random-effects meta-regressions to identify sources of study variance. 3 key findings →
Design: systematic review Participants: 3,562 Evidence: high
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After multivariable adjustment, patients showed an odds ratio (OR) 1·61 (95% CI 0·80-3·25) for scale 4 versus scale 3 and 4·60 (1·85-11·48) for scale 5-6 versus scale 3 for diffusion impairment; OR 0·88 (0·66-1·17) for scale 4 versus scale 3 and OR 1·77 (1·05-2·97) for scale 5-6 versus scale 3 for anxiety or depression, and OR 0·74 (0·58-0·96) for scale 4 versus scale 3 and 2·69 (1·46-4·96) for scale 5-6 versus scale 3 for fatigue or muscle weakness. 2 key findings →
Design: cohort study Participants: 94 Evidence: moderate
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Higher Hcy levels, lower educational attainment, and decreased physical activity were particularly strong predictors of incident AD. 3 key findings →
Design: systematic review Evidence: high
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We found up to 270-fold genetic enrichment between FTD and RA, up to 160-fold genetic enrichment between FTD and UC, up to 180-fold genetic enrichment between FTD and T1D, and up to 175-fold genetic enrichment between FTD and CeD. 5 key findings →
Design: meta-analysis Participants: 192,886 Evidence: low
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We tested whether dysregulation of cholesterol catabolism, through its conversion to primary bile acids (BAs), was associated with dementia pathogenesis. 5 key findings →
Design: cohort study Participants: 141 Evidence: moderate
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Intake of coffee alone or in combination with tea was associated with lower risk of poststroke dementia. 3 key findings →
Design: cohort study Participants: 365,682 Evidence: moderate
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Huperzine A is a Chinese herb extract used for Alzheimer's disease. 4 key findings →
Design: meta-analysis Participants: 1,823 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Increasing evidence suggests an association between pro-inflammatory diets and cognitive function. 4 key findings →
Design: cohort study Participants: 1,372 Evidence: moderate
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Epidemiological evidence regarding the association between atrial fibrillation (AF) onset age and risk of incident dementia remains unexplored. 4 key findings →
Design: cohort study Participants: 746 Evidence: moderate
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Higher dietary intakes of flavonols may be associated with reduced risk of developing Alzheimer dementia. 5 key findings →
Design: prospective cohort Participants: 691 Evidence: moderate
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Among the 286 autopsied brains of 544 participants, brain mercury levels were positively correlated with the number of seafood meals consumed per week (ρ = 0.16; P = .02). 5 key findings →
Design: cohort study Participants: 286 Evidence: moderate
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There are 9.9 million new cases of dementia in the world every year. 4 key findings →
Design: randomized controlled trial Participants: 52 Evidence: high
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Growing evidence suggests that fine particulate matter (PM 2.5 ) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. 5 key findings →
Design: cohort study Evidence: moderate
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The mean age was 70.9 years (standard deviation, 5.9), 57.2% were women, 40.6% were illiterate, and 88.3% were farmers. 2 key findings →
Participants: 5,765 Evidence: high
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While dementia affects 6-10% of persons 65 years or older, industrialized countries have witnessed an alarming rise in obesity. 2 key findings →
Design: systematic review Evidence: high
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By conditioning on the genetic association with the cardiovascular phenotypes, we identify novel AD susceptibility loci, including 2 genome-wide significant variants conferring increased risk for AD. 3 key findings →
Evidence: low
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Replication of these findings in a dietary intervention trial would be required to verify its relevance to brain health. 2 key findings →
Participants: 960 Evidence: low
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial surface receptor that triggers intracellular protein tyrosine phosphorylation. 4 key findings →
Evidence: low
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Our results depict that 5 Hz rTMS of the bilateral cerebellum is a promising, non-invasive treatment of cognitive dysfunction in AD patients. 4 key findings →
Participants: 27 Evidence: high
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Triggering receptor expressed on myeloid cells 2 (TREM2) is a microglial receptor that recognizes changes in the lipid microenvironment, which may occur during amyloid β (Aβ) accumulation and neuronal degeneration in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Plasma GFAP and pTau biomarkers (pTau181, pTau231, pTau217) are significantly elevated in Aβ-positive individuals, with stronger Aβ–pTau associations observed in APOE ε4 carriers (CPAS: β = 0.26, p = 0.003 for pTau231; ADNI: β = 0.45, p < 0.001 for pTau181). 5 key findings →
Design: cohort Participants: 806 Evidence: moderate
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Eight single-nucleotide polymorphisms (false discovery rate P Conclusions and relevance Our findings demonstrate genetic overlap between AD and immune-mediated diseases and suggest that immune system processes influence AD pathogenesis and progression. 2 key findings →
Design: longitudinal study Evidence: moderate
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Haplodeficiency of the microglia gene TREM2 increases risk for late-onset Alzheimer's disease (AD) but the mechanisms remain uncertain. 4 key findings →
Evidence: low
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Plasma metabolomic profile is disturbed in dementia patients, but previous studies have discordant conclusions. 4 key findings →
Participants: 24 Evidence: low
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Accumulating >300 min/week of MVPA, whether concentrated within 1-2 days or distributed evenly across the week, was associated with a decreased risk of dementia. 4 key findings →
Design: cohort Participants: 91,512 Evidence: moderate
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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.
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 →