28,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
The findings from the AHEAD Study screening process and longitudinal data from the LEARN Study are providing critical data to guide future prevention trial design. 5 key findings →
Design: longitudinal study Participants: 1,000 Evidence: moderate
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Higher ARTS score was associated (all ps < 0.01) with incident MCI (hazard ratio [HR] = 1.29), dementia (HR = 1.33), and stroke (HR = 1.52) and with diastolic/systolic blood pressure, self-reported hypertension, claudication, congestive heart failure, smoking, and glomerular filtration rate in the combined sample. 5 key findings →
Participants: 707 Evidence: low
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Our results highlight the prognostic value of biological AD staging. 5 key findings →
Participants: 492 Evidence: low
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Dietary influences on Alzheimer disease (AD) are gaining recognition. 1 key finding →
Evidence: low
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Macroautophagy/autophagy failure with the accumulation of autophagosomes is an early neuropathological feature of Alzheimer disease (AD) that directly affects amyloid beta (Aβ) metabolism. 4 key findings →
Evidence: low
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Progranulin (PGRN) is predominantly expressed by microglia in the brain, and genetic and experimental evidence suggests a critical role in Alzheimer's disease (AD). 4 key findings →
Evidence: low
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Subtype and Stage Inference (SuStaIn) is an unsupervised learning algorithm that uniquely enables the identification of subgroups of individuals with distinct pseudo-temporal disease progression patterns from cross-sectional datasets. 4 key findings →
Design: cross-sectional Evidence: low
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Although epidemiological data associate hypertension with a strong predisposition to develop Alzheimer disease, no mechanistic explanation exists so far. 4 key findings →
Evidence: low
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Clinical trials of anti-amyloid-β (Aβ) monoclonal antibodies in Alzheimer disease (AD) infer target engagement from Aβ positron emission tomography (PET) and/or fluid biomarkers such as cerebrospinal fluid (CSF) Aβ42/40. 2 key findings →
Evidence: moderate
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Older age was associated with greater odds of abnormal p-Tau217 (odds ratio [OR] 1.08 per year, 95% CI 1.07–1.09), as was APOE ε4 carrier status (OR 3.32, 95% CI 2.65–4.17). 5 key findings →
Design: cross-sectional Participants: 2,798 Evidence: moderate
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Polygenic risk scores (PRSs) predict an individual's genetic risk for complex diseases, yet their utility in elucidating disease biology remains limited. 1 key finding →
Evidence: low
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Measures of cognition were especially important predictive features of clinical diagnosis. 5 key findings →
Design: longitudinal study Evidence: moderate
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Current annual replacement cost of unpaid family care is between $96 and $182 billion, 44% of which is accounted for by dementia caregiving. 1 key finding →
Design: modelling Evidence: moderate
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Prior MR imaging studies, primarily at 1.5T, established hippocampal atrophy as a biomarker for Alzheimer disease. 3T MR imaging offers a higher contrast and signal-to-noise ratio, yet distortions and intensity uniformity are harder to control. 4 key findings →
Participants: 166 Evidence: low
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Severity of psychiatric symptoms, behavioral disturbances, and patients' quality of life are the main correlates of caregivers' experience burden. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The poor generalizability of clinical research data due to the enrollment of highly educated, non-Latinx White participants hampers the development of therapies for Alzheimer's disease (AD). 1 key finding →
Evidence: low
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'Amygdala' and 'amygdalar complex' are terms that now refer to a highly differentiated region near the temporal pole of the mammalian cerebral hemisphere. 5 key findings →
Evidence: low
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Microglia affect Alzheimer's disease (AD) pathogenesis in opposing manners, by protecting against amyloid accumulation in early phases of the disease and promoting neuropathology in advanced stages. 4 key findings →
Evidence: low
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Among TM enrollees, prevalence of dementia was lower by 4% points in 2014 (9.0%, 95%CI: 7.8%, 9.3%) compared to 2000 (13.0%, 95%CI: 12%, 14%). 5 key findings →
Design: cross-sectional Participants: 18,381 Evidence: low
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ε4, socioeconomic status, physical activity, smoking, subjective cognitive decline, and various cardiovascular risk factors and comorbidities. 4 key findings →
Design: cross-sectional Evidence: moderate
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The Centiloid method demonstrates strong intertracer and interscanner harmonization when standardized to the 11C-Pittsburgh compound B reference, with high correlation (r2 > 0.9) across 18F-labeled tracers, including florbetapir, flutemetamol, and florbetaben. 5 key findings →
Design: longitudinal study Evidence: moderate
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A total of 30 variants were overrepresented in four pathways: presenilin/Alzheimer disease, cadherin/WNT signaling, gonadotropin-releasing hormone receptor, and transforming growth factor-β (TGF-β) signaling. 5 key findings →
Participants: 204 Evidence: low
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All concurrent validity correlations followed the expected directionality, with 19/21 inter-scale correlations in the total sample reaching statistical significance (p<0.05), and 17/21 reaching at least a low correlation (0.3). 4 key findings →
Participants: 100 Evidence: low
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Higher GCA was associated with lower dementia risk (hazard ratio = 0.865, 95% confidence interval = 0.756 to 0.990). 5 key findings →
Evidence: low
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These findings provide no evidence of a group-level Alzheimer-related p-tau217 elevation in young people with DSRD and support DSRD as a condition distinct from Alzheimer’s disease. 5 key findings →
Design: longitudinal study Participants: 132 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 28,980 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 28,980 records, built mostly from automated pulls of Europe PMC (62.8% of the library) and OpenAlex (17.6%), 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.
1,038 records (3.6% of the library) are not peer-reviewed — 966 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 →