27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of 733 participants (mean age 82.5 ± 2.9 years), 164 (22.4%) developed MCI and 93 (12.7%) developed dementia by the follow-up visit. 5 key findings →
Design: longitudinal study Participants: 321 Evidence: moderate
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Researchers analyzed population-based data and relative risks from existing meta-analyses to estimate the population-attributable risk of Alzheimer's disease worldwide, in the USA, Europe, and the UK for seven potentially modifiable risk factors.
Evidence: low
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Evidence: low
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Among 1614 older adults (mean [SD] age, 66.3 [8.7] years; 980 women [60.7%]), 853 were Mexican American (mean [SD] age, 63.9 [7.9] years; 566 women [66.4%]), and 761 were non-Hispanic White (mean [SD] age, 69.1 [8.7] years; 414 women [54.4%]). 5 key findings →
Design: cross-sectional Participants: 280 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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Among 9239 eligible respondents, 5258 (57.7%) were female and 1210 (9.1%) were Black, 574 (4.7%) were Hispanic, and 7297 (84.4%) were White. 5 key findings →
Design: cohort study Evidence: moderate
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After adjusting for demographics, apolipoprotein E (APOE) ε4 status, cognition, and comorbidities, the highest tertile of REM latency was associated with higher Aβ burden (β = 0.08, 95% confidence interval [CI]: 0.03 to 0.13, p = 0.002), elevated p-tau181 (β = 0.19, 95% CI: 0.02 to 0.13, p = 0.002), and reduced BDNF levels (β = -0.47, 95% CI: -0.68 to -0.13, p = 0.013), compared to the lowest tertile. 5 key findings →
Participants: 128 Evidence: low
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Among the 1 268 599 participants (mean age, 73.9 [SD, 6.1] years; n = 25 335 [2%] female), dementia incidence rates per 1000 person-years were lowest in the Mid-Atlantic (11.2; 95% CI, 11.1-11.4) and highest in the Southeast (14.0; 95% CI, 13.8-14.2). 5 key findings →
Design: cohort study Participants: 25 Evidence: moderate
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We identify three distinct profiles: active healthy sleepers (AHS; 64.0%), fragmented poor sleepers (FPS; 14.1%), and long and frequent nappers (LFN; 21.9%). 3 key findings →
Design: cohort study Evidence: moderate
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Of 11 327 324 Medicare beneficiaries enrolled in hospice between 2010 and 2020 who met eligibility criteria (mean [SD] age, 85.2 [7.5] years; 781 763 [63.0%] female), there were 958 182 (8.4%) with a primary diagnosis of AD, 232 864 (2.1%) with PD, and 49 340 (0.4%) with DLB. 5 key findings →
Design: cohort study Evidence: moderate
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= 0.006). Univariable MR analyses indicated that education and participation reduced the risk of AD. 3 key findings →
Design: meta-analysis Evidence: high
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Higher BAG (pDeepBrainNet = 0.0002; pBrainAgeR = 0.00117) and lower hippocampal volume (p = 0.0015) and cortical thickness (p < 0.0001) were associated with worse clinical status (higher CDR). 2 key findings →
Participants: 2,870 Evidence: low
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We analyzed data from 3433 dementia-free participants with either magnetic resonance imaging or positron emission tomography (PET) data at baseline (mean [standard deviation] age: 65 [9] years, 36% non-Hispanic White [NHW], 27% Black, 37% Hispanic, and 63% women). 5 key findings →
Evidence: moderate
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We found a dose‐dependent association between ADI and dementia The ADI may be a valuable tool for identifying high‐risk communities for dementia intervention. 5 key findings →
Participants: 1,395,872 Evidence: low
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Using a large and diverse community‐based cohort, we demonstrate that ethno‐racial differences in AD‐specific plasma biomarkers are, in part, due to modifiable health and comorbidity factors. 2 key findings →
Participants: 931 Evidence: moderate
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Caregivers were on average 64 years old, 72% female, and 49% were the spouse of the patient (32% wives, 17% husbands). 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
Older age, White race, APOE ε4 carrier, and diabetes were associated with biomarker levels indicative of higher AD risk (lower Aβ42/40; higher p-tau217, p-tau217/Aβ42, NfL, and GFAP). 5 key findings →
Participants: 1,356 Evidence: low
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At baseline, 211 (3.6%) of the women had 6 or more depressive symptoms. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
All the five dimensional SDOH disadvantages were significantly associated with higher odds of both dementia and MCI in the overall sample (p <0.05) (Figure 1). 5 key findings →
Participants: 3,229 Evidence: low
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After adjusting for age, sex, race/ethnicity, education, APOE ε4, and physical activity, a greater multimorbidity burden (per 3 additional conditions) was associated with worse overall cognition (standardized β = -0.074, 95%CI -0.104 to -0.043) and biomarkers indicative of greater AD pathology, neurodegeneration, and SVD (Figure 1). 5 key findings →
Evidence: moderate
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After adjusting for age, sex, race/ethnicity, education, APOE ε4, and physical activity, a greater multimorbidity burden (per 3 additional conditions) was associated with worse overall cognition (standardized β =-0.074, 95%CI -0.104 to -0.043) and biomarkers indicative of greater AD pathology, neurodegeneration, and SVD (Figure 1). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
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 →