28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Sample 1 included 1656 participants (mean [range] age, 58.1 [29.7-85.6] years; 903 female [54.5%]), and sample 2 included 935 participants (mean [range] age, 67.6 [60.0-85.6] years; 518 female [55.4%]). 4 key findings →
Design: cohort study Participants: 1,656 Evidence: moderate
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APOE shows a heterogeneous effect on ADRD risk in our Hispanics/Latinos sample, the largest to date. 4 key findings →
Design: case-control Participants: 12,221 Evidence: moderate
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Importantly, they suggest that these associations might be explained by a decrease of amyloidosis and tau-pathology. 2 key findings →
Design: cross-sectional Participants: 512 Evidence: moderate
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The pooled sample comprised 4657 participants (30% women) aged ≥ 60 years (mean age was 74 years at sleep assessment). 5 key findings →
Design: cohort study Participants: 2,374 Evidence: moderate
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MarkVCID2 enrolled 1883 individuals age 73.4 ± 7.5 years, 65.0% female, 24.2% Hispanic, and 27.1% non-Hispanic Black. 5 key findings →
Design: longitudinal study Participants: 1,883 Evidence: moderate
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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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The study sample included 1,375 participants free of dementia and stroke at baseline (mean age 68 ± 6y, 54 % females). 5 key findings →
Design: cohort study Participants: 1,375 Evidence: moderate
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Comorbid cardiovascular and metabolic risk factors (CVM) differentially impact brain structure and increase dementia risk, but their specific magnetic resonance imaging signatures (MRI) remain poorly characterized. 1 key finding →
Design: cohort study Participants: 37,096 Evidence: moderate
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Inflammatory protein biomarkers induced by immune responses have been associated with cognitive decline and the pathogenesis of Alzheimer's disease (AD). 4 key findings →
Design: cross-sectional Participants: 708 Evidence: moderate
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The objective of this study was to investigate whether increased NLR in older adults is independently associated with the risk of subsequent dementia. 4 key findings →
Design: longitudinal study Participants: 1,648 Evidence: moderate
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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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These findings underscore the importance of blood pressure control in midlife to mitigate dementia risk. 5 key findings →
Participants: 229,976 Evidence: low
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-statistics 0.82-0.83). We found a significant association between all-cause dementia and multimarker CSVD scores, which was independent of the FSRP as well as its individual components. 3 key findings →
Design: cohort study Participants: 1,152 Evidence: moderate
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Longitudinal analysis identified significant associations between the change in ether lipid species (including alkylphosphatidylcholine, alkenylphosphatidylcholine, lysoalkylphosphatidylcholine, and lysoalkenylphosphatidylcholine) and AD dementia conversion. 5 key findings →
Design: cross-sectional Participants: 1,393 Evidence: moderate
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Three survey rounds included 49 to 54 participants that agreed on VasCog-2 diagnostic criteria for preclinical, mild, and major dementia levels of vascular cognitive impairment (under the overarching term VCID). 5 key findings →
Participants: 49 Evidence: low
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Caregiver stress is associated with negative outcomes for both caregivers and care recipients. 5 key findings →
Design: randomized controlled trial Participants: 14 Evidence: high
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Circulating metabolites were consistently associated with cognition, dementia, and lifestyle factors, opening new avenues for prevention of cognitive decline and dementia. 4 key findings →
Participants: 25,872 Evidence: low
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We found no statistically significant difference in measures of WM injury by race and ethnicity after adjustment for cardiovascular risk factors and socioeconomic status. 5 key findings →
Design: cross-sectional Participants: 1,036 Evidence: low
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We evaluated dementia-free Framingham Heart Study (generation 3) participants (mean age 48.5 years, 46.8% men) who underwent cognitive testing for memory, abstract reasoning, visual perception, attention, and executive function (n = 2,231) and brain MRI (n = 2018) to assess total white matter, lobar gray matter, and white matter hyperintensity volumes and fractional anisotropy (FA) measures. 4 key findings →
Participants: 2,231 Evidence: low
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Given the potential therapeutic effect of vascular disease control timing to reduce dementia risk, we investigated the age-related influences of vascular risk factor burden on brain structure throughout the lifespan. 4 key findings →
Design: cross-sectional Participants: 2,887 Evidence: moderate
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Higher structural stiffness of the carotid artery is associated with cognitive decline, whereas both structural and load‐dependent stiffness are associated with brain structural abnormalities common in Alzheimer disease‐related dementias. 5 key findings →
Design: cohort study Participants: 2,489 Evidence: moderate
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Cerebrovascular disease is the second most common cause of acquired cognitive impairment and dementia and contributes to cognitive decline in the neurodegenerative dementias. 5 key findings →
Evidence: low
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Amyloid PET imaging has been crucial for detecting the accumulation of amyloid beta (Aβ) deposits in the brain and to study Alzheimer's disease (AD). 4 key findings →
Participants: 13,409 Evidence: low
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Two of every three persons living with dementia reside in low- and middle-income countries (LMICs). 5 key findings →
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →