30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
The cohort sample included 5058 beneficiaries with dementia (mean [SD] age, 85.5 [8.0] years; 3038 women [60.1%]; 809 [16.0%] non-Hispanic Black, 357 [7.1%] Hispanic, and 3892 non-Hispanic White respondents [76.9%]). 4 key findings →
Design: cohort study Participants: 5,058 Evidence: moderate
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Patients with osteoarthritis had excess all cause mortality compared with the general population (standardised mortality ratio 1.55, 95% confidence interval 1.41 to 1.70). 2 key findings →
Design: cohort study Participants: 1,163 Evidence: moderate
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Each level increase in the severity of atherosclerosis or arteriolosclerosis was associated with significantly higher odds of Alzheimer's disease dementia (odds ratio [OR] for atherosclerosis 1·33, 95% CI 1·11-1·58; OR for arteriolosclerosis 1·20, 1·04-1·40). 4 key findings →
Design: cohort study Participants: 1,143 Evidence: moderate
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ADNI has demonstrated the feasibility and utility of multicenter PET studies and is helping to clarify the role of biomarkers in the study of aging and dementia. 3 key findings →
Design: longitudinal study Participants: 100 Evidence: moderate
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Our prediction model was internally evaluated based on five-fold cross-validation on discrimination and calibration, and it was further compared with existing prediction scales. 2 key findings →
Design: longitudinal study Participants: 2,416 Evidence: moderate
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If the associations we observed are causal, then air pollution from traffic might be an important risk factor for vascular dementia and Alzheimer's disease. 3 key findings →
Design: prospective cohort Participants: 1,806 Evidence: moderate
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The potential determinants of cognitive decline identified in this study, in particular modifiable risk factors, should be tested in the context of randomised controlled trials. 2 key findings →
Design: longitudinal study Participants: 626 Evidence: high
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For early detection of Alzheimer's disease, it is important to find biomarkers with predictive value for disease progression and clinical manifestations, such as cognitive decline. 1 key finding →
Design: longitudinal study Participants: 282 Evidence: moderate
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Increasing evidence suggests an important role of liver function in the pathophysiology of Alzheimer disease (AD). 4 key findings →
Design: cohort study Participants: 1,581 Evidence: moderate
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An increased tau positron emission tomography (PET) signal in the medial temporal lobe (MTL) has been observed in older individuals in the absence of amyloid-β (Aβ) pathology. 4 key findings →
Design: cohort study Participants: 1,093 Evidence: moderate
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MoCA was administered to 274 patients from 2 prospective hospital-based cohort studies in Germany (n = 125) and France (n = 149). 4 key findings →
Design: cohort study Participants: 125 Evidence: moderate
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In this single-center observational study, we included all individuals who visited the Alzheimer Center Amsterdam and had a clinical diagnosis of subjective cognitive decline (SCD), mild cognitive impairment (MCI), or probable AD dementia and were A+. 4 key findings →
Design: longitudinal study Participants: 520 Evidence: moderate
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The Alzheimer's Disease Neuroimaging Initiative (ADNI) is an ongoing, longitudinal, multicenter study designed to develop clinical, imaging, genetic, and biochemical biomarkers for the early detection and tracking of Alzheimer's disease (AD). 4 key findings →
Design: longitudinal study Participants: 400 Evidence: moderate
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Peripheral glial fibrillary acidic protein (GFAP) and neurofilament light chain (NfL) are sensitive markers of neuroinflammation and neuronal damage. 4 key findings →
Design: cohort study Participants: 48,542 Evidence: moderate
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The clinical value of current multifactorial algorithms for individualized assessment of dementia risk remains unclear. 4 key findings →
Design: cohort study Participants: 4,865 Evidence: moderate
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There were 21 603 to 51 236 patients per year (total for 2010-2020, 381 488 patients) in the OAC-eligible incident AF cohort (mean [SD] age, 77.2 [6.1] to 77.4 [6.8] years; 13 871 [51.8%] to 22 901 [49.8%] women). 5 key findings →
Design: cohort study Participants: 236 Evidence: moderate
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These findings provide evidence for a relationship between all types of alcohol use and increased dementia risk. 5 key findings →
Design: cohort Participants: 559,559 Evidence: moderate
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These findings add to growing evidence that women have a differential tau response to Aβ that may emerge at the point of p-tau secretion. 5 key findings →
Design: cohort Participants: 1,292 Evidence: moderate
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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
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In Alzheimer's disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration and cognitive decline. 3 key findings →
Design: cohort Participants: 609 Evidence: moderate
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The BioFINDER-2 main cohort included 872 participants, with an additional 156 participants in the Knight ADRC cohort for independent validation. 2 key findings →
Design: cohort Participants: 1,028 Evidence: high
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These results suggest that increasing levels of tau most consistently relate to declines in cognition preceding biomarker collection. 4 key findings →
Design: longitudinal study Participants: 152 Evidence: moderate
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Baseline plasma GFAP could detect abnormal CSF Aβ42/40 and CSF Aβ42/T-tau with an AUC of 0.79 (95% CI 0.72-0.86) and 0.80 (95% CI 0.72-0.86), respectively. 3 key findings →
Design: longitudinal study Evidence: moderate
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SUVr abnormality was most frequently observed in cingulate, followed by orbitofrontal, precuneal, and insular cortices and then the associative, temporal, and occipital regions. 1 key finding →
Design: longitudinal study Participants: 867 Evidence: moderate
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The clinical diagnosis of probable AD dementia demonstrated good agreement with biologically defined AD (positive predictive value 85.2%). 3 key findings →
Design: cohort study Participants: 166 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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.
1,037 records (3.4% of the library) are not peer-reviewed — 964 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events