28,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Comparison of probands with their unaffected spouses yielded odds ratios for AD of 9.9 (95% CI, 6.5 to 15.1) for head injury with loss of consciousness and 3.1 (2.3 to 4.0) for head injury without loss of consciousness. 3 key findings →
Participants: 2,233 Evidence: low
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Each additional copy of the apolipoprotein E4 (APOE4) allele is associated with a higher risk of Alzheimer's dementia, while the APOE2 allele is associated with a lower risk of Alzheimer's dementia, it is not yet known whether APOE2 homozygotes have a particularly low risk. 2 key findings →
Evidence: low
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Mean age was 73.5 years and mean HbA1c was 6.8%. 3 key findings →
Design: cohort study Evidence: moderate
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Chronic traumatic encephalopathy (CTE) is a neurodegeneration characterized by the abnormal accumulation of hyperphosphorylated tau protein within the brain. 2 key findings →
Evidence: low
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High WMH was a predictor of progression from normal to MCI (adjusted hazard ratio [HR], 3.30; 95% confidence interval [CI], 1.33-8.17; P= .01) but not conversion from MCI to all-cause dementia. 2 key findings →
Design: cohort study Participants: 67 Evidence: moderate
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The number of studies examining ECHO and ECHO-like models of medical tele-education has been modest compared with the scope and scale of implementation throughout the USA and internationally. 3 key findings →
Design: randomized controlled trial Evidence: high
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In a large community-based sample of middle-aged adults, BI predicted an increased risk of stroke and dementia independent of vascular risk factors. 5 key findings →
Participants: 1,694 Evidence: moderate
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The recycling of the amyloid precursor protein (APP) from the cell surface via the endocytic pathways plays a key role in the generation of amyloid beta peptide (Abeta) in Alzheimer disease. 4 key findings →
Evidence: low
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Age- and education-adjusted hazard ratios (HRs) for ADRD increased as neighborhood disadvantage increased, to 1.42 (95% confidence interval [CI] 1.06-1.91) in the most disadvantaged quintile compared to the least disadvantaged quintile, with a significant linear trend (p = 0.012). 5 key findings →
Design: longitudinal study Participants: 10,915 Evidence: moderate
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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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In this study, researchers assessed the validity and reliability of an automated labeling system developed to subdivide the human cerebral cortex on magnetic resonance images into gyral based regions of interest. 3 key findings →
Evidence: low
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Researchers developed an adeno-associated virus-based model to study tau propagation from the entorhinal cortex to the dentate gyrus. 2 key findings →
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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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Long-term use of sulfonylureas, thiazolidinediones, or insulin was not associated with an altered risk of developing AD. 3 key findings →
Design: case-control study Evidence: moderate
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Selective survival of men with a healthier cardiovascular risk profile and hence lower propensity to dementia might partly explain the higher LTR of dementia/AD in women. 1 key finding →
Participants: 7,901 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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Of the 2,183 participants (mean ± SD age 79 ± 4.5 years, 58% female, 24% Black), 176 (8%) developed dementia. 5 key findings →
Design: cohort study Participants: 2,183 Evidence: moderate
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This study included 10 333 FHS 5 key findings →
Design: cohort study Participants: 886 Evidence: moderate
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A total of 42 342 participants from the pooled cohorts were included (mean [SD] age, 61.3 [9.8] years; 55.0% female). 5 key findings →
Design: cohort study Participants: 342 Evidence: moderate
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This study examined a transgenic mouse model in which human tau P301L overexpression was restricted to layer II of the entorhinal cortex (EC-II). 4 key findings →
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Our ancestry-aware regression approach showed that AA individuals have a lower risk of AD if they inherited African ancestry admixture block at the 17p13.2 locus. 5 key findings →
Design: case-control Participants: 10,271 Evidence: moderate
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We used magnetic resonance imaging (MRI) measurements to determine whether persons in the prodromal phase of Alzheimer's disease (AD) could be accurately identified before they developed clinically diagnosed dementia. 1 key finding →
Participants: 24 Evidence: low
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The LTR of stroke in middle-aged adults is 1 in 6 or more, which is equal to or greater than the LTR of AD. 3 key findings →
Participants: 4,897 Evidence: moderate
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Reversible phase separation underpins the role of FUS in ribonucleoprotein granules and other membrane-free organelles and is, in part, driven by the intrinsically disordered low-complexity (LC) domain of FUS. 2 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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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 →