30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Common genetic variance in apolipoprotein E (APOE), β-glucocerebrosidase (GBA), microtubule-associated protein tau (MAPT), and α-synuclein (SNCA) has been linked to cognitive decline in Parkinson's disease (PD), although studies have yielded mixed results. 4 key findings →
Design: longitudinal study Participants: 281 Evidence: moderate
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Alzheimer's disease is one of the most heritable diseases in elderly people and the most common type of dementia. 4 key findings →
Design: cohort study Participants: 926 Evidence: moderate
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We identified 4 novel genetic loci that implicate inflammatory and glial proliferative pathways in the development of WMH in addition to previously proposed ischemic mechanisms. 2 key findings →
Design: meta-analysis Participants: 17 Evidence: high
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PurposeTelephone disclosure of genetic test results can improve access to services. 4 key findings →
Participants: 257 Evidence: high
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This study aimed to evaluate the impact of APOE4 homozygosity on Alzheimer's disease (AD) by examining its clinical, pathological and biomarker changes to see whether APOE4 homozygotes constitute a distinct, genetically determined form of AD. 2 key findings →
Participants: 3,297 Evidence: low
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These findings provide evidence for a relationship between all types of alcohol use and increased dementia risk. 5 key findings →
Design: cohort Participants: 559,559 Evidence: moderate
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The large number of participants screened with amyloid positron emission tomography (PET) and standardized assessments provides an unprecedented opportunity to evaluate factors associated with elevated brain amyloid. 5 key findings →
Design: cross-sectional Participants: 4,486 Evidence: low
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Brain DNA methylation in multiple AD loci is associated with AD pathologies. 5 key findings →
Design: cohort study Participants: 447 Evidence: moderate
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Brain iron elevation is implicated in Alzheimer's disease (AD) pathogenesis, but the impact of iron on disease outcomes has not been previously explored in a longitudinal study. 3 key findings →
Design: longitudinal study Evidence: moderate
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A variant within a DNase hypersensitive site 5' of TREM2, rs9357347-C, associates with reduced AD risk and increased TREML1 and TREM2 levels (uncorrected P = 6.3 × 10 -3 and 4.6 × 10 -2 , respectively). 4 key findings →
Design: meta-analysis Participants: 1,006 Evidence: high
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We sent invitations to 91,433 households; 5542 (6.1%) responded, 2120 completed the Baseline Survey (78.5% online; 21.5% via computer-assisted telephone interview), and 2087 were deemed eligible, yielding a response rate of 2.3%. 2 key findings →
Design: randomized controlled trial Participants: 374 Evidence: high
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Data from 3960 MRI sessions among 1141 participants were included: 252 pathogenic variant carriers from DIAN (mean [SD] age, 38.4 [11.2] years; 137 [54%] female), 571 older adults from ADNI (mean [SD] age, 72.8 [7.3] years; 274 [48%] female), and 318 older adults from HABS (mean [SD] age, 72.4 [7.6] years; 194 [61%] female). 3 key findings →
Design: cohort study Participants: 1,141 Evidence: moderate
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A substantial proportion of the relationship between education and dementia was mediated through mid-life vascular risk factors. 2 key findings →
Design: cohort Participants: 13,368 Evidence: moderate
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Early tau deposition was elevated in women compared with men in individuals on the Alzheimer disease trajectory. 5 key findings →
Design: cross-sectional Participants: 89 Evidence: low
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At 48 months, group differences between clinical progressors and non-progressors were significant for self (2.13, SE=0.45, P Conclusions and relevance Demonstrating long-term clinical benefit will be critical for the success of recently launched secondary prevention trials. 1 key finding →
Design: longitudinal study Participants: 468 Evidence: moderate
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Frontotemporal lobar degeneration (FTLD) is the second most common cause of presenile dementia. 1 key finding →
Participants: 515 Evidence: low
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Cognitive decline is a debilitating manifestation of disease progression in Parkinson's disease. 4 key findings →
Design: longitudinal study Participants: 3,200 Evidence: moderate
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Researchers conducted a large, two-stage meta-analysis of genome-wide association studies in individuals of European ancestry.
Evidence: low
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APOE4 is the strongest genetic risk factor for late-onset Alzheimer disease. 5 key findings →
Evidence: low
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In ADNI, Aβ-positive participants showed more decline than did Aβ-negative participants with regard to the ADCS-PACC score at 24 months (mean [SE] difference, -1.239 [0.522] [95% CI, -2.263 to -0.215]; P = .02). 4 key findings →
Evidence: low
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Estimates of AD disease duration become more accurate if age, sex, setting, APOE, and cerebrospinal fluid tau are taken into account. 2 key findings →
Participants: 3,268 Evidence: low
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High Aβ participants were more likely to be APOE ε4+ than low Aβ participants. 2 key findings →
Design: cohort study Evidence: moderate
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Sample 1 included 1656 participants (mean [range] age, 58.1 [29.7-85.6] years; 903 female [54.5%]), and sample 2 included 935 participants (mean [range] age, 67.6 [60.0-85.6] years; 518 female [55.4%]). 4 key findings →
Design: cohort study Participants: 1,656 Evidence: moderate
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Meta-analysis of the 2 family-based and the 5 case-control cohorts yielded a p value of 0.0029, while the overall summary estimate (using case-control data only) resulted in an odds ratio of 1.67 (95% confidence interval 0.95-2.92) for the association between the TREM2 R47H and increased AD risk. 3 key findings →
Design: meta-analysis Evidence: high
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Genetic risk factors of AD dementia demonstrate effects related to Aβ, as well as synergistic interactions with Aβ. 2 key findings →
Design: longitudinal study Participants: 702 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. 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,040 records (3.4% of the library) are not peer-reviewed — 965 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events