27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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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The 2,641 participants had a mean (SD) age of 74 (2.8) years at baseline; 53 % were female, 36 % were of Black race, and had a range of baseline CKM: 3 % Stage 0 (no CKM), 4 % Stage 1 (excess/dysfunctional adiposity), 26 % Stage 2 (metabolic risk factors), 24 % Stage 3 (subclinical CVD and CKD), and 43 % Stage 4 (clinical CVD and CKD). 5 key findings →
Design: cohort study Participants: 3,075 Evidence: moderate
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Of the total of 1795 subjects randomized in Clarity AD, 294 subjects were in the Asian region (Japan:152; Korea:129; Singapore:13). 5 key findings →
Design: clinical trial Participants: 294 Evidence: high
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Self- and informant-reported ADL and IADL impairments were examined at overall and item levels. 3 key findings →
Design: longitudinal study Participants: 1,050 Evidence: moderate
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Addressing modifiable dementia risk factors requires reliable risk assessment methods. 2 key findings →
Design: meta-analysis Evidence: high
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The GBT model achieved the best AUC-ROC scores of 0.809-0.833 across 1- to 5-year prediction windows. 4 key findings →
Design: case-control study Participants: 380,269 Evidence: moderate
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After the intervention, the CG showed significantly lower scores compared to all experimental groups. 4 key findings →
Design: randomized controlled trial Participants: 92 Evidence: high
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The average detection rates for mild cognitive impairment is 0.08 (interquartile range=0.00-0.02) for both clinicians and practices, suggesting that only about 8% of expected cases were diagnosed on average. 3 key findings →
Participants: 25 Evidence: low
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. Longitudinally, older age (OR=1.14 [1.06-1.22], p<.001), higher levels of p-tau217 (OR=10.37 [3.00-35.02], p<.001) and higher neuropsychiatric symptoms (OR=1.19 [1.02-1.39], p=.023) were associated with higher odds of progression to dementia. 5 key findings →
Design: cross-sectional Participants: 104 Evidence: moderate
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Of 2,218 participants, 237 (11%) developed dementia in the period 1992/3 to 2015/6. 5 key findings →
Design: cohort study Participants: 2,218 Evidence: moderate
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Low baseline Aβ42/Aβ40 was significantly associated with increased amyloid accumulation (β = 0.257, 95% confidence interval (CI) 0.177-0.336, P < 0.001), and with higher risk of conversion to Aβ-PET positivity (Hazard ratio (HR) = 2.84, 95% CI 1.14-7.04, P = 0.025) and to MCI due to AD (HR = 3.25, 95% CI 1.17-9.01, P = 0.024). 5 key findings →
Design: longitudinal study Participants: 200 Evidence: moderate
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Of 104 metabolites studied, glycodeoxycholic acid (GDCA) surpassed the false discovery rate and was associated the Alzheimer's Disease Assessment Scale-Cognitive Subscale version 13 (ADAS-Cog13) score (β = 0.12, 95 % CI = 0.05-0.20, p = 0.001) and cognitive impairment determined by mini-mental status exam (MMSE) (OR = 2.11, 95 % CI = 1.41-3.15, p < 0.001). 4 key findings →
Design: cross-sectional Participants: 578 Evidence: moderate
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- Cognition was assessed with the Ruff Figural Fluency Test (RFFT), measuring non-verbal fluency and executive functioning. 5 key findings →
Design: cohort study Participants: 23,798 Evidence: moderate
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Compared with the control arm (n = 36), the TEAM-V Program (n = 39) was associated with significantly improved general cognition (MoCA, P = 0.02) at 2 years. 5 key findings →
Design: longitudinal study Participants: 40 Evidence: high
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Significant interactions between amyloid status and modifiable risk factors were observed for diabetes (adjusted β = -0.206, p = 0.032), high cholesterol (adjusted β = -0.155, p < 0.001), and physical inactivity (adjusted β = -0.161, p = 0.046), indicating combined effects rather than additive effects on cognitive decline among Aβ+ individuals. 5 key findings →
Design: cohort study Participants: 1,707 Evidence: moderate
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Among 331,731 participants (mean ± SD age, 56.53 ± 8.1 years; 156,762 [47.26 %] male), 4413 (1.33 %) developed dementia during a mean follow-up of 12.8 years. 5 key findings →
Design: cohort study Participants: 331,731 Evidence: moderate
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• Low ALPS index was significantly associated with high risk of MCI, and the risk of MCI decreased linearly with a higher ALPS index • High ALPS index was dose-dependently associated with a decreased progression from MCI to AD • High ALPS index may delay the MCI onset approximately 3.8 years among CN participants and delay MCI progression to AD by approximately 3.5 years in MCI group • Aβ in choroid plexus, tau in part of the cortex and executive function were partially mediate ALPS-AD association We aimed to explore the association between ALPS index and both risks of MCI from cognitively normal (CN) and incident AD progressed from MCI, as well as potential mediating factors. 1 key finding →
Participants: 519 Evidence: moderate
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Non-modifiable (age, apolipoprotein E (APOE) ɛ4 genotype and sex) and modifiable risk factors (co-morbidities at baseline, such as hypertension and cardiovascular disease, BMI, and sleep duration) were analyzed with mixed-effects models, adjusted for age and sex, to predict longitudinal measurements of WMH, Aβ and tau. 5 key findings →
Design: longitudinal study Participants: 494 Evidence: moderate
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Over a follow-up period of 6.2 years, 513 participants were diagnosed with dementia. 5 key findings →
Design: cohort study Participants: 513 Evidence: moderate
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In the whole population (N = 1,214,286) and the subpopulation (N = 88,565), 5 % had no risk factors, 12 % had only one, and 82 % had multiple. 4 key findings →
Design: cross-sectional Participants: 1,214,286 Evidence: moderate
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ADI groups differed by sex, ethnoracial background, and MMSE scores. 5 key findings →
Design: cohort study Participants: 755 Evidence: moderate
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Among 5,145 participants included in the analyses, 747 (14.5 %) reported hearing loss, including 207 Black adults and 199 White adults. 5 key findings →
Design: cohort study Participants: 5,145 Evidence: moderate
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The national combined PAF for 11 modifiable risk factors was 39.6 % (95 % CI: 20.8-55.9). 5 key findings →
Design: cross-sectional Participants: 86,494 Evidence: low
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We identified 132,968 individuals, of whom 12,088 with severe Zoster, 60,440 matched controls among the general population, and 60,440 matched controls among the hospitalised population. 5 key findings →
Participants: 132,968 Evidence: moderate
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A total of 43,160 participants were included (mean [standard deviation] age, 64.2 [7.7] years, 53.1 % female). 5 key findings →
Design: cross-sectional Participants: 43,160 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. 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 →