27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
We provide evidence for 16 novel AD loci and advocate for more studies using whole genome sequencing-based GWAS of diverse cohorts. 4 key findings →
Design: meta-analysis Participants: 432,374 Evidence: moderate
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New PRSs for dementia significantly improve risk-prediction performance, but still account for less risk than APOE genotype overall. 3 key findings →
Design: cohort Participants: 12,031 Evidence: moderate
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Pittsburgh Compound B PET findings match histopathologic reports of beta-amyloid (Abeta) distribution in aging and dementia. 2 key findings →
Design: longitudinal study Evidence: moderate
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A higher level of total daily physical activity is associated with a reduced risk of AD. 4 key findings →
Design: cohort study Participants: 71 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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The agreement between Aβ classification with CSF Aβ42 and 18F-flutemetamol positron emission tomography was very high (κ = 0.85). 3 key findings →
Design: cross-sectional Participants: 118 Evidence: moderate
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Within-person changes in CSF biomarkers were also compared with changes in cortical PiB binding and progression to a CDR higher than 0 at follow-up. 2 key findings →
Design: cohort study Participants: 169 Evidence: moderate
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The relationship between serum total cholesterol (TC) and dementia seems to be bidirectional. 5 key findings →
Design: longitudinal study Participants: 1,449 Evidence: moderate
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The APOE epsilon4 allele is a genetic risk factor for dementia with stroke, including VaD and AD with CVD. 5 key findings →
Design: case-control study Participants: 187 Evidence: moderate
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However, the clinical presentation, associated factors, frequency in community-based cohorts, genetic characteristics, and cognitive trajectories associated with the quadruple misfolded proteins phenotype are not well understood. 5 key findings →
Design: cohort study Participants: 375 Evidence: moderate
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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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The (11)C-PiB-PET imaging results demonstrated reduction of fibrillar Aβ accumulation in patients with Alzheimer disease treated with bapineuzumab; however, as no clinical benefit was observed, the findings are consistent with the hypotheses that bapineuzumab may not have been initiated early enough in the disease course, the doses were insufficient, or the most critical Aβ species were inadequately targeted. 4 key findings →
Design: clinical trial Participants: 115 Evidence: low
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Delirium is an acute change in cognition, common in hospitalized older adults, and associated with high healthcare and human cost; however, delirium's genetic and proteomic background remains poorly understood. 4 key findings →
Design: meta-analysis Participants: 1,059,130 Evidence: high
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Alzheimer's disease (AD) is a debilitating, chronic neurodegenerative disease. 2 key findings →
Design: meta-analysis Evidence: high
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Both environmental exposures and genetics are known to play important roles in shaping human aging. 5 key findings →
Participants: 492,567 Evidence: low
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We found that common variation at the CR1 locus has a broad impact on cognition and that this effect is largely mediated by an individual's amyloid plaque burden. 4 key findings →
Design: cohort study Participants: 1,666 Evidence: moderate
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Amyotrophic lateral sclerosis (ALS) is a multi-system disease characterized primarily by progressive muscle weakness. 2 key findings →
Design: longitudinal study Participants: 327 Evidence: moderate
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Most people's cognitive abilities decline with age, with significant and partly genetically driven, individual differences in rate of change. 3 key findings →
Design: longitudinal study Participants: 1,087 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Combining human cohort data (over 24,000 people) with mouse models, this study found that carrying the APOE2 gene variant is linked to a longer lifespan, and that this benefit holds even when accounting for Alzheimer's diagnosis and brain pathology. 4 key findings →
Design: cohort Participants: 24,661 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alongside APOE ε4, iPRS-DEM may refine risk stratification for the enrichment of dementia clinical trials and prevention programs. 3 key findings →
Design: cohort Participants: 241,935 Evidence: moderate
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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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Dementia is a frequent problem encountered in advanced stages of Parkinson disease (PD). 5 key findings →
Design: longitudinal study Evidence: moderate
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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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These results suggest that the inheritance of APOE epsilon 4 is associated with reduced cerebral parietal metabolism and increased asymmetry in non-demented relatives at risk for probable AD. 4 key findings →
Design: longitudinal study Participants: 12 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 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 →