27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Surrogates were accurate in the majority of cases, made errors in 12% to 22% of cases, and were uncertain in 11% to 16% of cases. 4 key findings →
Design: longitudinal study Evidence: moderate
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Percentages of patients with imaging tests, DLB symptoms, diagnoses and treatments for DLB increased as patients’ first DLB diagnosis neared and occurred at lower percentages 7‐12 months after initial diagnosis. 1 key finding →
Design: systematic review Participants: 974 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Participants in the most disadvantaged neighborhoods (n = 156) were younger, more often female, and less often college-educated or white than those in less disadvantaged neighborhoods (n = 1963). 3 key findings →
Participants: 156 Evidence: low
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Hypertension, hypercholesterolemia, obesity, and diabetes were overrepresented in AA participants, but were not associated with cognitive impairment. 5 key findings →
Participants: 261 Evidence: low
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Considerable variations of breadth and intensity in county-level HCBS were observed. 4 key findings →
Participants: 365,310 Evidence: low
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The mean (SD) age of the 4,631 participants was 67.6 (4.89) years, and 2579 (55.7%) were women. 5 key findings →
Design: cross-sectional Participants: 4,943 Evidence: low
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Exposure to high neighborhood‐level socioeconomic disadvantage is associated with negative health outcomes. 5 key findings →
Design: longitudinal study Participants: 645 Evidence: moderate
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SNF discharges decreased while home and HHA discharges increased during the pandemic. 5 key findings →
Participants: 830,656 Evidence: moderate
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We found that both state of birth and state of residence account for a modest portion of ADRD mortality variation. 5 key findings →
Design: longitudinal study Evidence: moderate
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Alzheimer's disease (AD) neuropathology is extremely heterogeneous, and the evolution from preclinical to mild cognitive impairment until dementia is driven by interacting genetic/biological mechanisms not fully captured by current clinical/research criteria. 2 key findings →
Participants: 20 Evidence: low
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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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Neighborhood disadvantage was associated with worse cognitive performance on memory, executive function, processing speed, and preclinical Alzheimer's tests on both datasets. 5 key findings →
Participants: 524 Evidence: moderate
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The sample (n = 26,728) was equally distributed across gender (55.1% women) and education (50.8% completed HS/GED diploma), and 30% came from under-represented racial/ethnic groups. 5 key findings →
Design: cross-sectional Participants: 26,728 Evidence: low
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Our study included 74,275 weeks of driving data (2015-2024, average follow-up 6.1 years). 5 key findings →
Design: longitudinal study Participants: 36 Evidence: moderate
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A significant ADI × dementia interaction was observed for global atrophy (p = .005) and several other outcomes. 5 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
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The empirical language composite showed superior and consistent sensitivity (faster decline rate) with all three biomarkers. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
= 0.81). NfL levels were not significantly associated with GDS-15 in a population of community-dwelling older adults without dementia. 4 key findings →
Design: cross-sectional Participants: 512 Evidence: low
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This cohort study examines the association of serum hyperphosphorylated tau and neurofilament light chain concentrations with psychosis in Alzheimer disease. 1 key finding →
Design: cohort study Evidence: moderate
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= 0.006). Univariable MR analyses indicated that education and participation reduced the risk of AD. 3 key findings →
Design: meta-analysis Evidence: high
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In their study, Chen et al 1 examined the association between apolipoprotein E (APOE) genotype and longitudinal cognitive trajectories among middle-aged and older East Asian adults participating in the Healthy Aging Longitudinal Study of Taiwan (HALST).Although sporadic late-onset Alzheimer disease (AD) is polygenic, APOE remains the strongest genetic determinant of AD risk, with carriers of the APOE ε4 allele having increased odds of developing AD dementia in a dose-dependent manner compared with APOE ε3 homozygotes. 1 key finding →
Design: longitudinal study Participants: 21 Evidence: moderate
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< 0.001). This study suggests 2 molecular pathways underlying CAA, with a larger effect size for the pathway including SFRP1 and APOE protein and C-terminally truncated Aβ before position 40. 2 key findings →
Design: cross-sectional Evidence: low
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This cross-sectional study examines lecanemeb update among Medicare fee-for-service beneficiaries with Alzheimer disease or mild cognitive impairment and evaluates whether there are disparities among potentially eligible patients. 1 key finding →
Design: cross-sectional Evidence: low
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Three trajectory classes were identified: stable, slow decliners, and fast decliners. 4 key findings →
Design: longitudinal study Evidence: moderate
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Four thousand four hundred eighty-six participants were included (mean age 71.3 ± 4.7 years, 30% participants Aβ+, 59% female). 5 key findings →
Design: cross-sectional Evidence: moderate
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This narrative review examines the utility of gait digital biomarkers in Parkinson's disease (PD) research and clinical trials across four contexts: disease susceptibility/risk, disease progression, response to exercise, and fall prediction. 1 key finding →
Design: narrative review 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.
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 →