27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Risk for late-onset Alzheimer's disease (LOAD), the most prevalent dementia, is partially driven by genetics. 5 key findings →
Design: meta-analysis Participants: 94,437 Evidence: high
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The double-cutoff approach revealed high confidence for interpreting scans as negative when Centiloid values were lower than 11 (95% CI, 9-13; I2 = 95%) and interpreting scans as positive if Centiloid values were higher than 26 (95% CI, 24-28; I2 = 95%). 3 key findings →
Design: meta-analysis Participants: 49,227 Evidence: high
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APOE ɛ4, the most significant genetic risk factor for Alzheimer disease (AD), may mask effects of other loci. 5 key findings →
Design: meta-analysis Participants: 4,203 Evidence: high
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Using cross-population GWAS meta-analyses, we identify novel LOAD susceptibility loci in/near LRRC4C and LHX5-AS1, both with known roles in neuronal development, as well as several novel population-unique loci. 1 key finding →
Design: meta-analysis Participants: 409,589 Evidence: high
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Analysis confirmed the association of APOE with earlier AAO (P = 3.3 × 10(-96)), with associations in CR1 (rs6701713, P = 7.2 × 10(-4)), BIN1 (rs7561528, P = 4.8 × 10(-4)), and PICALM (rs561655, P = 2.2 × 10(-3)) reaching statistical significance (P Conclusions and relevance We confirmed an association of APOE (OMIM 107741) variants with AAO among affected participants with LOAD and observed novel associations of CR1 (OMIM 120620), BIN1 (OMIM 601248), and PICALM (OMIM 603025) with AAO. 3 key findings →
Design: meta-analysis Participants: 9,162 Evidence: high
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In a pooled sample of multiple selected cohorts of cognitively unimpaired older adults, higher plasma p-tau217 levels were consistently associated with increased risk of clinical progression and accelerated cognitive decline. 5 key findings →
Design: cohort Participants: 2,684 Evidence: high
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Across the brain, people with Down syndrome had greater concentrations of tau for a given level of amyloid compared with people with autosomal-dominant Alzheimer's disease. 3 key findings →
Design: cohort study Participants: 137 Evidence: moderate
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APOE shows a heterogeneous effect on ADRD risk in our Hispanics/Latinos sample, the largest to date. 4 key findings →
Design: case-control Participants: 12,221 Evidence: moderate
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Alzheimer's disease (AD) is a progressive neurodegenerative disease with a complex and heterogeneous pathophysiology. 4 key findings →
Evidence: low
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Each additional copy of the apolipoprotein E4 (APOE4) allele is associated with a higher risk of Alzheimer's dementia, while the APOE2 allele is associated with a lower risk of Alzheimer's dementia, it is not yet known whether APOE2 homozygotes have a particularly low risk. 2 key findings →
Evidence: low
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Global PET amyloid burden was compared with regards to cognitive status, APOE ɛ4 status, sex, age, and estimated years to symptom onset. 2 key findings →
Design: cross-sectional Participants: 216 Evidence: low
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Among 1614 older adults (mean [SD] age, 66.3 [8.7] years; 980 women [60.7%]), 853 were Mexican American (mean [SD] age, 63.9 [7.9] years; 566 women [66.4%]), and 761 were non-Hispanic White (mean [SD] age, 69.1 [8.7] years; 414 women [54.4%]). 5 key findings →
Design: cross-sectional Participants: 280 Evidence: moderate
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Plasma p-tau217 concentrations, considered together with APOE genotype, might help stratify risk and estimate the timing of future cognitive impairment in asymptomatic individuals who are at increased risk for Alzheimer's disease, such as those with a family history of dementia or known APOE-ε4 carrier status. 5 key findings →
Design: cohort Participants: 8,582 Evidence: high
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These results suggest that all adults with Down syndrome should be screened for Alzheimer's disease pathology starting shortly before age 40 years and considered for clinical trials. 1 key finding →
Design: longitudinal study Participants: 328 Evidence: moderate
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During the past decade, a conceptual shift occurred in the field of Alzheimer's disease (AD) considering the disease as a continuum.
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For both cohorts, the prevalence of mosaicism was 40 and Aβ 42 concentrations. 2 key findings →
Design: longitudinal study Participants: 357 Evidence: moderate
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No large-scale characterizations of neurofilament light chain (NfL) have been conducted in diverse populations. 1 key finding →
Participants: 890 Evidence: low
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Depression is a known risk factor for dementia and MCI, but its associations with AT(N) biomarkers remain inconsistent and may differ by cognitive status. 4 key findings →
Design: longitudinal study Participants: 2,929 Evidence: moderate
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Our findings highlight the value of transethnic studies for identifying novel AD susceptibility loci. 3 key findings →
Evidence: low
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The Alzheimer's Association hosted the second Latinos & Alzheimer's Symposium in May 2021. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Alzheimer's disease (AD) is a complex genetic disorder with no effective treatments. 4 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Microglial activation participates in white matter injury after cerebral hypoperfusion. 4 key findings →
Participants: 80 Evidence: low
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Arch Neurol. 2008;65(7):963-967.) for the Mini-Mental State Examination in detecting cognitive dysfunction in a bilingual sample of highly educated ethnically diverse individuals. 4 key findings →
Participants: 7,093 Evidence: moderate
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The characteristics of the cohort revealed significant groupwise differences in age, education, sex, and cognitive diagnosis. 5 key findings →
Evidence: moderate
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Higher BAG (pDeepBrainNet = 0.0002; pBrainAgeR = 0.00117) and lower hippocampal volume (p = 0.0015) and cortical thickness (p < 0.0001) were associated with worse clinical status (higher CDR). 2 key findings →
Participants: 2,870 Evidence: low
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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 →