27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
After 3.5 years of follow up, 19 new cases of dementia were identified among 229 surviving participants. 5 key findings →
Design: cohort study Participants: 341 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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The incidence of dementia was 0.68 (95% CI 0.64-0.72) cases per 100 person-years in pSS, and it was 0.58 (0.56-0.60) in the controls. 5 key findings →
Design: cohort study Participants: 20,160 Evidence: moderate
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At least 45% of dementia and 60% of stroke cases are due to modifiable risk factors and could in part be prevented through healthy behavior. 3 key findings →
Design: cross-sectional Participants: 1,478 Evidence: moderate
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ATTRACTnet was developed in an internal test set of 799 patients (mean [SD] age, 75.1 [11.1] years; 516 [64.7%] male and 283 [35.3%] female) using 5-fold cross-validation with an additional external test set of 422 patients. 5 key findings →
Design: open-label trial Participants: 799 Evidence: high
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Age, education level, number of pain sites, pain duration, pain level, depression and sleep quality were risk factors of MCI in older patients with chronic pain. 5 key findings →
Design: longitudinal study Participants: 612 Evidence: moderate
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Distinct gut microbial compositions are associated with dementia. 2 key findings →
Design: systematic review Participants: 896 Evidence: high
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Early detection of Alzheimer's disease (AD) is critical yet challenging, particularly in younger individuals. 1 key finding →
Design: longitudinal study Participants: 120 Evidence: moderate
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Between Sept 1, 2017, and Feb 28, 2019, 19 403 individuals were invited to participate and 9745 participants (1525 with dementia, 8220 without dementia) were included. 4445 (45·6%) of 9745 participants were male and 5300 (54·4%) were female. 5 key findings →
Design: cohort study Participants: 403 Evidence: moderate
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We used an untargeted mass spectrometric approach, tandem mass tag proteomics, for the identification of proteomic signatures in genetic frontotemporal dementia (FTD). 5 key findings →
Participants: 238 Evidence: low
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During an average follow-up of 3.63 years, we observed a total of 1 493 individuals developing dementia among 4 341 depressed and 43 214 matched non-depressed individuals (62.4% female; mean [SD] age at baseline 64.4 [11.1] years). 5 key findings →
Design: longitudinal study Participants: 493 Evidence: moderate
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Plasma p‐tau217 has clinical, neuroimaging, and neuropathological correlates in sporadic FTD and may identify FTD cases with AD co‐pathology. 1 key finding →
Design: longitudinal study Participants: 620 Evidence: moderate
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NPS was longitudinally associated with performance in each cognitive domain. 5 key findings →
Design: longitudinal study Participants: 1,247 Evidence: moderate
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Prevention of dementia represents a public health priority. 3 key findings →
Design: longitudinal study Participants: 180 Evidence: moderate
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The data of 508,107 individuals were analyzed (mean [standard deviation] age, 67.6 [10.7] years; 66.8% women and 33.2% men), and 39,318 developed Alzheimer's disease (22,572 controls and 16,746 using aspirin). 5 key findings →
Design: cohort study Participants: 508,107 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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A single-timepoint ResNet3D model achieved modest performance (c-index ~ 0.70). 5 key findings →
Design: longitudinal study Evidence: moderate
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Among 1,528,885 adults with type 2 diabetes (mean age, 58 years; 49.2% women), GLP-1 receptor agonists plus metformin were associated with lower incidence of vascular dementia (HR, 0.46; 95% CI, 0.37-0.57), mild cognitive disorder (HR, 0.79; 95% CI, 0.66-0.95), and Alzheimer disease (HR, 0.46; 95% CI, 0.31-0.70). 5 key findings →
Design: cohort study Participants: 1,528,885 Evidence: moderate
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MEDAS-R was positively associated with better MMSE performance (p = 0.043) and showed a borderline association with the MoCA (p = 0.051), but not with the ACE-R score (p = 0.356). 5 key findings →
Design: randomized controlled trial Participants: 75 Evidence: high
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In frontotemporal dementia and amyotrophic lateral sclerosis, the RNA-binding protein TDP-43 is depleted from the nucleus of neurons in the brain and spinal cord. 2 key findings →
Evidence: low
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Chronological age is an imperfect estimate of molecular aging. 5 key findings →
Participants: 4,018 Evidence: low
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Based on data from their first NACC visit with AD, there was considerable heterogeneity in language performance across people with EOAD and LOAD. 5 key findings →
Design: cross-sectional Participants: 1,189 Evidence: low
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The study sample included 3566 Black (16 104 observations) and 17 555 White (90 874 observations) participants. 5 key findings →
Design: cross-sectional Participants: 3,566 Evidence: low
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Alzheimer's disease (AD) is the leading cause of dementia and is characterized by progressive amyloid accumulation followed by tau-mediated neurodegeneration. 1 key finding →
Evidence: low
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Our results suggest that microstructural features derived from NODDI such as fISO might be useful adjunct markers to tau, which needs to be confirmed in longitudinal studies. 2 key findings →
Design: longitudinal study Participants: 80 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.
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 →