27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Among persons without dementia, the prevalence of cerebral amyloid pathology as determined by positron emission tomography or cerebrospinal fluid findings was associated with age, APOE genotype, and presence of cognitive impairment. 4 key findings →
Design: meta-analysis Participants: 2,914 Evidence: high
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The likelihood of amyloid positivity was associated with age and APOE ε4 status. 3 key findings →
Design: meta-analysis Participants: 377 Evidence: high
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Enrollment was undertaken between May 18, 2021, and September 8, 2023. 2 key findings →
Design: clinical trial Participants: 210 Evidence: high
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Frontotemporal dementia (FTD) is a complex disorder characterised by a broad range of clinical manifestations, differential pathological signatures, and genetic variability. 4 key findings →
Design: meta-analysis Participants: 3,526 Evidence: high
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A total of 95 unique studies were included in this systematic review, of which 74 with 2 760 379 unique patients were also included in 5-year age band meta-analyses. 5 key findings →
Design: systematic review Participants: 95 Evidence: high
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Circulating NfL and GFAP may, independently and jointly, provide useful clinical insight regarding dementia risk and prognosis. 4 key findings →
Design: cohort Participants: 1,712 Evidence: moderate
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Of 92 383 participants, 60 582 (65.6%) were women and the mean (SD) age was 56.4 (8.0) years. 3 key findings →
Design: cohort Participants: 92,383 Evidence: moderate
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The results of this cohort study suggest that hearing loss was associated with increased dementia risk, especially among people not using hearing aids, suggesting that hearing aids might prevent or delay the onset and progression of dementia. 5 key findings →
Design: cohort Participants: 573,088 Evidence: moderate
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Observationally, CVDs were associated with risk of all incident outcomes in meta-analyses, with hazard ratios up to 7.00 (95% confidence interval [CI]: 6.20, 7.92). 5 key findings →
Design: meta-analysis Participants: 10,373 Evidence: high
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We found no significant association for exposure to nitrogen oxides (five studies, n=241 409, pooled adjusted HR per 10 μg/m 3 increase, 1·05 [0·97-1·13]; I 2 =44%), PM 10 (four studies, n=246 440, pooled adjusted HR per 15 μg/m 3 increase, 1·52 [0·80-2·87]; I 2 =82%), or annual ozone (four studies, n=419 972, pooled adjusted HR per 45 μg/m 3 increase, 0·82 [0·35-1·92]; I 2 =69%), with moderate to considerable heterogeneity between studies in these pooled analyses. 5 key findings →
Design: meta-analysis Participants: 24,030,527 Evidence: moderate
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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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Additionally, our results indicate that AD subjects carrying APOE ε4 are more responsive to the neuroprotective effects of physical activity. 3 key findings →
Design: randomized controlled trial Evidence: high
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A total of 450 111 participants were included in the study (mean [SD] age, 51.1 [9.8] years; 70.8% women) and followed up during a median (IQR) time of 14.9 (4.1) years. 5 key findings →
Design: cohort study Participants: 111 Evidence: moderate
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Growing evidence suggests that fine particulate matter (PM 2.5 ) likely increases the risks of dementia, yet little is known about the relative contributions of different constituents. 5 key findings →
Design: cohort study Evidence: moderate
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Sleep is a fundamental biological process with broad implications for physical and mental health, yet its complex relationship with disease remains poorly understood. 5 key findings →
Participants: 65,000 Evidence: low
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The overall PAF for dementia in Denmark was 37·8% (95% CI 35·6-40·0) for the assessed risk factors. 4 key findings →
Design: cohort Participants: 1,753,515 Evidence: high
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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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A polygenic score (PGS) for Alzheimer's disease (AD) was derived recently from data on genome-wide significant loci in European ancestry populations. 4 key findings →
Design: cohort Evidence: high
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A single-question screen for RBD may reliably detect disease, with psychometric properties favorably comparable to those reported for longer questionnaires. 2 key findings →
Design: case-control study Evidence: moderate
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In the new AA diagnostic criteria, AD can be defined clinically as encompassing cognitively normal people having a core 1 AD biomarker. 5 key findings →
Evidence: low
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The genetic variant rs72824905-G (minor allele) in the PLCG2 gene was previously associated with a reduced Alzheimer's disease risk (AD). 4 key findings →
Participants: 53,627 Evidence: low
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As the brain transitions from wakefulness to sleep, processing of external information diminishes while restorative processes, such as glymphatic removal of waste products, are activated. 5 key findings →
Evidence: early
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The quality of included studies with only a few longitudinal studies, limits the conclusions which may be drawn from the present findings especially regarding the biomarkers other than hippocampal volume. 4 key findings →
Design: systematic review Participants: 40 Evidence: high
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Low plasma levels of apoE are associated with increased risk of future Alzheimer disease and all dementia in the general population, independent of ε2/ε3/ε4 APOE genotype. 3 key findings →
Participants: 75,708 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 →