Median follow-up by intention to treat was 2.0 years. 2 key findings →
Participants: 1,180 Evidence: low
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27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Median follow-up by intention to treat was 2.0 years. 2 key findings →
Participants: 1,180 Evidence: low
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Among 10 095 participants (67.3% men; aged 35-55 years in 1985-1988), a total of 1710 cases of diabetes and 639 cases of dementia were recorded over a median follow-up of 31.7 years. 3 key findings →
Design: cohort study Participants: 95 Evidence: moderate
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Masitinib is an orally administered tyrosine kinase inhibitor that targets activated cells of the neuroimmune system (mast cells and microglia). 4 key findings →
Participants: 182 Evidence: high
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This study suggests that plasma GFAP is a sensitive biomarker for detecting and tracking reactive astrogliosis and Aβ pathology even among individuals in the early stages of AD. 5 key findings →
Design: cross-sectional Participants: 300 Evidence: moderate
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Median follow-up increased from 2.0 years in the double-blind trial to 3.9 years overall. 2 key findings →
Participants: 1,485 Evidence: high
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Amyloid-beta 42 (Aβ42) and phosphorylated tau (pTau) levels in cerebrospinal fluid (CSF) reflect core features of the pathogenesis of Alzheimer's disease (AD) more directly than clinical diagnosis. 2 key findings →
Participants: 8,074 Evidence: low
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During 1 110 831 person-years at risk, we recorded 245 573 hospitalisations in the Finnish cohorts; the corresponding numbers in the UK study were 60 946 hospitalisations in 186 572 person-years. 4 key findings →
Design: cohort study Participants: 9,838 Evidence: moderate
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Midlife and late-life risk factors contributed to 22.7% and 16.5% of total dementia cases, respectively. 5 key findings →
Design: meta-analysis Participants: 37,931 Evidence: high
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Adherence to the Life Simple 7 ideal cardiovascular health recommendations in midlife was associated with a lower risk of dementia later in life. 4 key findings →
Design: cohort study Participants: 7,899 Evidence: moderate
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More frequent social contact at age 60 years was associated with lower dementia risk (hazard ratio [HR] for each SD higher social contact frequency = 0.88 [95% CI 0.79, 0.98], p = 0.02); effect size of the association of social contact at 50 or 70 years with dementia was similar (0.92 [95% CI 0.83, 1.02], p = 0.13 and 0.91 [95% CI 0.78, 1.06], p = 0.23, respectively) but not statistically significant. 3 key findings →
Design: cohort Participants: 10,228 Evidence: moderate
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Sleep dysregulation is a feature of dementia but it remains unclear whether sleep duration prior to old age is associated with dementia incidence. 4 key findings →
Participants: 7,959 Evidence: low
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However, the importance of detailed cognitive phenotyping in patients without dementia when interpreting p-tau217 results remains unclear. 4 key findings →
Design: cohort study Participants: 2,323 Evidence: moderate
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Multimorbidity (hazard ratio [HR] 4·12 [95% CI 3·41-4·98]), frailty (HR 2·38 [95% CI 1·93-2·93]), and disability (HR 1·73 [95% CI 1·34-2·22]) were associated with increased risk of mortality; these associations were not modified by socioeconomic status. 2 key findings →
Design: cohort study Participants: 308 Evidence: moderate
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The clinical value of current multifactorial algorithms for individualized assessment of dementia risk remains unclear. 4 key findings →
Design: cohort study Participants: 4,865 Evidence: moderate
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Among 12,327 patients who underwent randomization (6162 to the asundexian group and 6165 to the placebo group), the incidence of ischemic stroke was lower in the asundexian group than in the placebo group (6.2% vs. 8.4%; cause-specific hazard ratio, 0.74; 95% confidence interval [CI], 0.65 to 0.84; P<0.001). 5 key findings →
Design: clinical trial Participants: 12,327 Evidence: low
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In this genetic association study, a novel variant associated with AD was identified: R251G always coinherited with ε4 on the APOE gene, which mitigates the ε4-associated AD risk. 5 key findings →
Design: case-control study Participants: 37 Evidence: moderate
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A total of 704 records met the inclusion criteria for bibliometric analysis. 5 key findings →
Design: systematic review Participants: 704 Evidence: high
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Our findings suggest that decreasing disparities between sexes in education, due to secular increases in educational opportunities, could attenuate sex differences in dementia risk and cognitive decline in the future. 1 key finding →
Design: cohort study Participants: 924 Evidence: moderate
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Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. 2 key findings →
Evidence: low
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Alzheimer disease comorbid pathologic characteristics are common and are associated with more rapid cognitive decline in patients with dementia with Lewy bodies (DLB); therefore, it is anticipated that plasma p-tau concentrations may have utility in assessing cognitive impairment in individuals with this disorder. 4 key findings →
Design: cohort study Participants: 371 Evidence: moderate
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The ε4 allele of apolipoprotein E (APOE) gene and increasing age are two of the most important known risk factors for developing Alzheimer disease (AD). 4 key findings →
Design: cohort study Participants: 1,593 Evidence: moderate
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Female participants had a lower hazard of early-onset dementia compared with males (HR 0·70 [95% CI 0·61-0·80]). 4 key findings →
Design: cohort Participants: 544,442 Evidence: high
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All synaptic biomarkers tested had a good discriminatory power to distinguish patients with AD abnormal CSF from those with non-AD disorders. 4 key findings →
Design: cross-sectional Participants: 81 Evidence: moderate
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Among 137 randomized participants, 2 were excluded for not meeting eligibility criteria, leaving 135 (mean [SD] age, 69.3 [3.8] years; 83 female [61%]) eligible for analysis. 3 key findings →
Design: randomized controlled trial Evidence: high
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The Preferred Reporting Items for Systematic reviews and Meta-Analyses (PRISMA) statement, published in 2009, was designed to help systematic reviewers transparently report why the review was done, what the authors did, and what they found.
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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 →