30,980 Alzheimer's and dementia studies in plain English, each scored out of 100.
Lower baseline amyloid beta (Aβ)42/40 ratio and higher phosphorylated tau 181 (p-tau181), glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) were associated with an increased risk of MCI and dementia; GFAP was most strongly associated. 5 key findings →
Participants: 2,467 Evidence: high
Full summary, score breakdown and related studies → Original source
Plasma biomarkers of AD neuropathology, neuronal injury, and astrogliosis increase with age and are associated with known dementia risk factors. 5 key findings →
Design: cohort Participants: 1,525 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
The Japan-Multimodal Intervention Trial for Prevention of Dementia PRIME Tamba (J-MINT PRIME Tamba) is a randomised controlled trial to prevent cognitive decline in community-dwelling cognitively ordinary older people at risk of dementia. 2 key findings →
Design: randomized controlled trial Participants: 200 Evidence: high
Full summary, score breakdown and related studies → Original source
Midlife measurement of plasma Aβ may have utility as a blood-based biomarker indicative of risk for future cognitive impairment. 4 key findings →
Design: cohort study Participants: 2,284 Evidence: moderate
Full summary, score breakdown and related studies → Original source
The mean (SD) baseline age of 758 participants was 61.5 (6.1) years, and 424 participants [55.9%] were female. 4 key findings →
Design: cohort study Participants: 758 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Circulating NfL and GFAP may, independently and jointly, provide useful clinical insight regarding dementia risk and prognosis. 4 key findings →
Design: cohort Participants: 1,712 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Among the 1453 participants in the Framingham dementia study sample, the mean (SD) age was 75 (7) years; 792 (54.5%) were female. 3 key findings →
Design: cohort study Participants: 1,453 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
This study suggests that the prognostic capacity of plasma NfL may be amplified in individuals with Aβ or hypertension. 5 key findings →
Design: longitudinal study Participants: 720 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Across the cohorts, each 10-year increase in BAI was associated with a 39% higher risk of incident dementia (hazard ratio [HR], 1.39 [95% CI, 1.21-1.59]; P Conclusions and relevance In this IPD meta-analysis, a higher sleep EEG-based BAI was associated with a higher risk of incident dementia. 3 key findings →
Design: meta-analysis Participants: 7,105 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
High and increasing blood pressure from early adulthood into midlife seems to be associated with increased WMHV and smaller brain volumes at 69-71 years of age. 5 key findings →
Design: longitudinal study Participants: 5,362 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Higher concentrations of plasma p-tau217, p-tau181, and NfL were correlated to higher decline speed of Mini-Mental State Examination score, and higher risk of incident dementia and AD. 3 key findings →
Design: longitudinal study Participants: 1,857 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Of 6256 participants (3402 women [54.4%]; mean [SD] age at baseline, 61.7 [6.6] years), 510 received an all-cause dementia diagnosis within 17 years of baseline. 3 key findings →
Design: cohort study Participants: 766 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Overall, 2,277 individuals had at least 1 baseline blood biomarker available (n = 357 for CSF subsample, n = 649 for PET subsample), among whom 257 were diagnosed with clinical AD/mixed dementia during follow-up. 2 key findings →
Design: prospective cohort Participants: 357 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
At baseline, 2,279 dementia-free participants with available blood samples were included (median age 72 (interquartile range, 61-81) years; 62% female). 4 key findings →
Design: cohort Participants: 2,279 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Biomarkers were measured in 431 Black and 583 White participants (mean age of 77 and 80 years and 17% and 21% of men, respectively), generating a balanced sample of 366:366. 3 key findings →
Design: cohort Participants: 1,014 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
A total of 3363 adults were enrolled in SNAC-K (73.3% participation rate). 5 key findings →
Design: cohort study Participants: 3,363 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Elevated levels of AD biomarker p-tau181/Aβ42, by itself or combined with a low Aβ42/Aβ40 level, predicts clinically diagnosed AD. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Type 2 diabetes is associated with altered plasma concentrations of Aβ peptides and is an important source of variation that needs to be taken into account when considering plasma Aβ peptides as biomarkers for Alzheimer's disease. 4 key findings →
Participants: 194 Evidence: moderate
Full summary, score breakdown and related studies → Original source
However, chronic cardiovascular risk factors such as diabetes and hypertension are associated with plasma biomarker levels and can influence the accurate prediction of underlying neuropathologic changes. 2 key findings →
Design: case-control study Evidence: moderate
Full summary, score breakdown and related studies → Original source
These factors should be investigated in longitudinal studies for their role in detecting onset of symptoms in AD. 1 key finding →
Design: longitudinal study Participants: 749 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
The data set included 18 178 patients, of which 10 991 (60.5%) had MCI and 7187 (39.5%) had dementia (mean [SD] age, 75.8 [6.3] years; 9333 women [51.3%]). 3 key findings →
Design: cross-sectional Participants: 18 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood-based biomarkers of AD/ADRD are influenced by common demographic and clinical characteristics. 2 key findings →
Participants: 779 Evidence: high
Full summary, score breakdown and related studies → Original source
Measurement of tau in serum is feasible. 2 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
BackgroundDiabetes has been linked to increased prevalence of dementia, but the link between diabetic retinopathy (DR) and Alzheimer's disease (AD) remains unclear. 4 key findings →
Design: cross-sectional Participants: 79 Evidence: low
Full summary, score breakdown and related studies → Original source
These findings suggest that increases in certain plasma AD biomarkers are associated with NP in WLWH and WLWOH and may be associated with later onset of AD, and measuring these biomarkers could be a pivotal advancement in monitoring aging brain health and development of AD among women with and without HIV. 5 key findings →
Design: cohort study Participants: 307 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 30,980 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 30,980 records, built mostly from automated pulls of Europe PMC (65.2% of the library) and OpenAlex (16.4%), 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.
1,042 records (3.4% of the library) are not peer-reviewed — 967 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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