31,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We tested whether dysregulation of cholesterol catabolism, through its conversion to primary bile acids (BAs), was associated with dementia pathogenesis. 5 key findings →
Design: cohort study Participants: 141 Evidence: moderate
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Among 34 349 participants, 19 378 individuals who were free of stroke and dementia and had longitudinal BP, cognitive, and covariate data were included in the analysis. 2 key findings →
Design: longitudinal study Participants: 349 Evidence: moderate
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In this exploratory analysis of a US community-based cohort, several echocardiographic measures of lower LA function were significantly associated with an increased risk of subsequent dementia. 5 key findings →
Design: prospective cohort Participants: 4,096 Evidence: moderate
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Head injury was associated with risk of dementia (hazard ratio [HR] = 1.44, 95% confidence interval [CI] = 1.3-1.57), with evidence of dose-response (1 head injury: HR = 1.25, 95% CI = 1.13-1.39, 2+ head injuries: HR = 2.14, 95% CI = 1.86-2.46). 3 key findings →
Design: cohort study Participants: 14,376 Evidence: moderate
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Studies were significantly heterogeneous in terms of country, outcomes assessed, and the timing of post-ED outcome assessments. 5 key findings →
Design: systematic review Participants: 7,940 Evidence: high
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Among 13,875 individuals with nonmissing VRF and outcome data with up to 30 years of follow-up (25% Black, 54% female), 179 developed PD at a mean age of 73.4 years, 94 developed PDD at a mean age of 79.2 years, and 1,791 developed dementia without PD at a mean age of 79.7 years. 5 key findings →
Design: longitudinal study Participants: 13,875 Evidence: moderate
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A substantial proportion of the relationship between education and dementia was mediated through mid-life vascular risk factors. 2 key findings →
Design: cohort Participants: 13,368 Evidence: moderate
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Diabetes increased the risk of conversion to dementia. 2 key findings →
Design: meta-analysis Evidence: high
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The development of MCI is associated with measurements of cognition and depression, racial and constitutional factors, and cerebrovascular disease. 5 key findings →
Design: longitudinal study Participants: 927 Evidence: moderate
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From October 2018 to March 2020, 58 participants were recruited (29 per group, 95% [86%-99%]). 5 key findings →
Design: randomized controlled trial Participants: 58 Evidence: high
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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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Stroke, dementia, and hypertension are associated with late-onset epilepsy; however, the role of other vascular and lifestyle factors remains unclear. 5 key findings →
Design: cohort study Participants: 792 Evidence: moderate
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The objective is to identify risk factors associated with PASC/long-COVID diagnosis. 5 key findings →
Design: case-control study Participants: 8,325 Evidence: moderate
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Of the 14 685 participants (7355 female [50%] and 7330 male [50%]; mean [SD] age, 73.8 [8.5] years) who met the inclusion criteria, 221 participants (1.5%) developed LOE during follow-up. 5 key findings →
Design: longitudinal study Participants: 713 Evidence: moderate
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= 0.009). Significant differences in annualized changes in these FA and MD values were found depending on the presence or absence of type 2 diabetes and smoking. 4 key findings →
Design: longitudinal study Participants: 6,471 Evidence: moderate
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Secondary analysis suggested that this effect may be driven primarily by individuals who are negative for the established AD genetic risk factor, apolipoprotein E (APOE) ɛ4. 5 key findings →
Design: case-control study Participants: 346 Evidence: moderate
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More-severe diabetes (defined by higher HbA 1c and longer disease duration) but not prediabetes or less-severe diabetes was associated with smaller brain volumes and an increased burden of brain vascular pathology. 3 key findings →
Design: cross-sectional Participants: 1,713 Evidence: low
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Classification resulted in 227 persons with prevalent dementia at entry into the study and 480 incident cases during follow-up. 4 key findings →
Design: cohort study Participants: 227 Evidence: moderate
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The CHS has developed a methodology for longitudinal studies of dementia in large cohorts and represents the largest study of dementia including cognitive testing, MRI and genetic markers. 1 key finding →
Design: longitudinal study Participants: 5,888 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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While dementia affects 6-10% of persons 65 years or older, industrialized countries have witnessed an alarming rise in obesity. 2 key findings →
Design: systematic review Evidence: high
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Sex differences in major cardiovascular risk factors for incident (fatal or non-fatal) all-cause dementia were assessed in the UK Biobank. 4 key findings →
Participants: 502,226 Evidence: low
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A total of 368 participants were included (median [IQR] age, 58 [50-65] years; 71% were female, 27% were Black, 6% were Hispanic, and 61% were White; median [IQR] BMI, 32.3 [28.5-37.1]). 5 key findings →
Design: clinical trial Participants: 368 Evidence: high
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Incidence of all-cause dementia is very high in people aged 90 years and older and continues to increase exponentially with age in both men and women. 2 key findings →
Design: longitudinal study Evidence: moderate
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Diabetes status, poor glycemic control, and longer diabetes duration were associated with worse cognitive outcomes over a median follow-up of 5 years. 4 key findings →
Participants: 5,099 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 31,780 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 31,780 records, built mostly from automated pulls of Europe PMC (66% of the library) and OpenAlex (16%), 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.
1,052 records (3.3% of the library) are not peer-reviewed — 973 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 →
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