27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Further studies are warranted to develop and refine the specific MIND diet for different populations. 4 key findings →
Design: meta-analysis Participants: 224,049 Evidence: moderate
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The mean age of 634 patients was 80 years. 3 key findings →
Participants: 6,838 Evidence: high
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The study enrolled 181 participants (mean [SD] age, 69.6 [7.2] years; 114 [63.0%] female): 91 to the intervention arm (depression in later life [DIL] intervention) and 90 to care as usual (CAU). 1 key finding →
Participants: 181 Evidence: high
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Compared with respective matched nonusers, individuals receiving haloperidol had an increased mortality risk of 3.8% (95% CI, 1.0%-6.6%; P Conclusions and relevance The absolute effect of antipsychotics on mortality in elderly patients with dementia may be higher than previously reported and increases with dose. 5 key findings →
Design: case-control study Participants: 90,786 Evidence: moderate
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Those reporting depressive symptoms in 1985 (mean follow-up, 27 years) did not have significantly increased risk for dementia (hazard ratio [HR], 1.21; 95% CI, 0.95-1.54) in Cox regression adjusted for sociodemographic covariates, health behaviors, and chronic conditions. 5 key findings →
Design: cohort study Participants: 322 Evidence: moderate
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There were 987 participants (290 from Vantaa 85+, 241 from the Cambridge City Over-75s Cohort, and 456 from the Cognitive Function and Ageing Study) with neuropathologic data; mean (SD) age at death was 90 (6.4) years, including 682 women (69%). 5 key findings →
Design: cohort study Participants: 987 Evidence: moderate
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Low-dose aspirin did not prevent depression in this large-scale study of otherwise healthy older adults. 3 key findings →
Participants: 114 Evidence: high
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The analytic cohort included 2488 black and white older adults with repeated depressive symptom assessments from baseline to year 5 who were free of dementia throughout that period. 4 key findings →
Design: prospective cohort Participants: 1,322 Evidence: moderate
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Subjective cognitive decline (SCD) is recognized to be in the Alzheimer disease (AD) cognitive continuum. 4 key findings →
Design: cohort study Participants: 3,585 Evidence: moderate
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Of 486 older adults who provided consent, 375 (with rMDD, MCI, or both) received at least 1 intervention session (mean [SD] age, 72.2 [6.4] years; 232 women [62%] and 143 men [38%]). 3 key findings →
Evidence: high
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Late-life depression (LLD) is characterized by considerable heterogeneity in clinical manifestation. 4 key findings →
Design: longitudinal study Participants: 996 Evidence: moderate
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Although the presence of abnormal levels of amyloid-β (Aβ) is associated with higher rates of progression to clinically classified mild cognitive impairment or dementia, little research has evaluated potentially modifiable moderators of Aβ-related cognitive decline, such as anxiety and depressive symptoms. 5 key findings →
Design: cohort study Participants: 333 Evidence: moderate
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Most studies have focused on dementia and suicidal behavior, with inconsistent results. 5 key findings →
Design: cohort study Participants: 21 Evidence: moderate
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Cerebral amyloid-β aggregation is an early event in Alzheimer disease (AD). 4 key findings →
Design: cross-sectional Participants: 2,908 Evidence: low
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Expression profiles of amacrine cells (interneurons within the retina) were robustly enriched in schizophrenia genetic risk across mammalian species and in different developmental stages. 5 key findings →
Design: cohort study Participants: 36 Evidence: moderate
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In the longitudinal analysis of p-tau181 trajectories of the AD+P group, the group of patients who showed incidence of psychosis over the course of follow-up (AD+P incident) demonstrated an associated increase in plasma p-tau181 levels compared with the group of patients who had psychosis at baseline (AD+P baseline) and showed an associated decrease in plasma p-tau181 levels (F4, 117 = 3.24; P = .01). 4 key findings →
Design: cohort study Participants: 752 Evidence: moderate
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Loneliness is a perceived state of social and emotional isolation that has been associated with cognitive and functional decline and an increased risk of incident AD dementia. 5 key findings →
Design: cross-sectional Participants: 25 Evidence: low
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Salience network hyperconnectivity may be a distinguishing feature in children with ASD. 2 key findings →
Design: case-control study Evidence: moderate
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In this study's cohort of 155 individuals with SETRS (mean [SD] age, 59.3 [10.3] years; 56 female participants [36.1%]), 153 of 155 (98.7%) scored below the cutoff of 26 for mild cognitive impairment, and 73 of 155 (47.1%) scored below the cutoff of 10 for severe dementia (mean [SD] MoCA score, 9.8 [6.4]). 5 key findings →
Design: cohort study Participants: 155 Evidence: moderate
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The analysis involved 4674 participants (2904 [62.13%] female and 1770 [37.87%] male; mean [SD] age, 41.51 [13.41] years). 5 key findings →
Participants: 906 Evidence: low
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The CSF levels of Aβ42 but not total and phosphorylated tau were lower in APOE ε4 carriers compared with noncarriers irrespective of diagnostic group (cohort A). 3 key findings →
Participants: 105 Evidence: moderate
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Of 10 974 participants (60.0% female, mean [SD] age: 73.2 [6.8] years), 2445 developed incident all-cause dementia over 116 067 person-years of follow-up. 5 key findings →
Participants: 974 Evidence: moderate
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Most patients with svMCI do not exhibit substantial amyloid burden, and CVD does not increase β-amyloid burden as measured by amyloid imaging. 5 key findings →
Design: cross-sectional Participants: 95 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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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 →