32,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Concentrations of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years before expected symptom onset. 5 key findings →
Design: cross-sectional Participants: 128 Evidence: moderate
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Mean age was 83.5 (SD, 8.5) years in cohort 1, 69.1 (SD, 10.3) years in cohort 2, and 35.8 (SD, 10.7) years in cohort 3; 38% were women in cohort 1, 51% in cohort 2, and 57% in cohort 3. 4 key findings →
Design: cross-sectional Participants: 301 Evidence: moderate
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This study suggests that plasma GFAP is a sensitive biomarker for detecting and tracking reactive astrogliosis and Aβ pathology even among individuals in the early stages of AD. 5 key findings →
Design: cross-sectional Participants: 300 Evidence: moderate
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Neurofilament light chain (NfL) is a promising fluid biomarker of disease progression for various cerebral proteopathies. 2 key findings →
Design: cross-sectional Participants: 187 Evidence: moderate
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Participants had a mean (SD) age of 66.9 (9.9) years; 971 (33.3%) were Aβ positive by either CSF or PET, 1667 (57.2%) were women, and 1108 (38.1%) carried at least 1 APOE ε4 allele. 5 key findings →
Design: cross-sectional Participants: 2,916 Evidence: high
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Plasma p-tau217/Aβ42 has high performance in detecting cerebral AD pathologies, thus offering a promising tool for clinical diagnosis and community screening of AD. 1 key finding →
Design: cross-sectional Participants: 512 Evidence: moderate
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The mean (SD) age of the 842 participants in cohort 1 was 72 (5.6) years, with a range of 59 to 88 years, and 446 (52.5%) were female. 3 key findings →
Design: cross-sectional Participants: 842 Evidence: moderate
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For all 4 phosphorylation sites assessed in CSF, p-tau was significantly more closely associated with amyloid-PET values than tau-PET values (p-tau181 difference, 13%; 95% CI, 3%-22%; P = .006; p-tau217 difference, 11%; 95% CI, 3%-20%; P = .003; p-tau231 difference, 15%; 95% CI, 5%-22%; P Conclusions and relevance Results of this cross-sectional study of 2 observational cohorts suggest that the p-tau abnormality as an early event in AD pathogenesis was associated with amyloid-β accumulation and highlights the need for careful interpretation of p-tau biomarkers in the context of the amyloid/tau/neurodegeneration, or A/T/(N), framework. 2 key findings →
Design: cross-sectional Participants: 609 Evidence: moderate
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This study found that CSF-based estimates using adjusted data-driven cutoffs were up to 10% higher than PET-based estimates in people without dementia, whereas the results were similar among people with dementia. 3 key findings →
Design: cross-sectional Participants: 97 Evidence: moderate
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CKD was associated with increased p-tau217 concentrations when measuring p-tau217 by ALZpath and C 2 N methodologies, but the effect was mitigated by the use of %p-tau217. 5 key findings →
Design: cross-sectional Participants: 202 Evidence: moderate
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Higher eGFR was associated with increased levels of plasma p-tau217, p-tau181, Tau212-221, and Tau181-190 in individuals with cognitive impairment (cohort 1: R range, -0.24 to -0.59; P Conclusions and relevance In this study, CKD was associated with increased plasma levels of soluble tau, but for p-tau217 the associations were considerably lower than the association with Aβ positivity. 4 key findings →
Design: cross-sectional Participants: 141 Evidence: moderate
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The large number of participants screened with amyloid positron emission tomography (PET) and standardized assessments provides an unprecedented opportunity to evaluate factors associated with elevated brain amyloid. 5 key findings →
Design: cross-sectional Participants: 4,486 Evidence: low
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There were 838 BioFINDER-2 participants (mean age, 73.9 [SD, 7.3] years; 431 women [51%]; 407 men [49%]) and 380 ADNI participants (average age, 72.9 [SD, 7.0] years; 194 women [51%]; 186 mean [49%]) included. 3 key findings →
Design: cross-sectional Participants: 838 Evidence: moderate
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Serum NfL concentration is increased in FAD prior to symptom onset and correlates with measures of disease stage and severity. 3 key findings →
Design: cross-sectional Participants: 48 Evidence: low
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Plasma NfL is superior to plasma t-tau for the diagnosis and prediction of clinical progression of FTLD-S and AD-S. Classification of evidence This study provides Class III evidence that plasma NfL has superior diagnostic and prognostic performance vs plasma t-tau in FTLD and AD. 2 key findings →
Design: cross-sectional Participants: 265 Evidence: moderate
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The use of an amyloid clock enabled visualization and analysis of biomarker changes as a function of estimated years from symptom onset in sporadic AD. 1 key finding →
Design: cross-sectional Participants: 118 Evidence: moderate
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In DIAD, solanezumab was not associated with ARIA. 5 key findings →
Design: cross-sectional Participants: 52 Evidence: moderate
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Plasma p-tau217/Aβ42 had high accuracy to detect AD, with comparable performance across race. 2 key findings →
Design: cross-sectional Participants: 1,135 Evidence: moderate
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While APOEε4 is associated with increased amyloid-β burden, its association with cerebral tau pathology has been controversial. 5 key findings →
Design: cross-sectional Participants: 124 Evidence: moderate
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Among 300 participants with DS and a control group of 37 non-DS siblings, mean (SD) age was 45.0 (10.1) years, and 167 (49.6%) were men. 4 key findings →
Design: cross-sectional Participants: 300 Evidence: low
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Sleep duration is linked to amyloid-β clearance while physical activity is associated with brain volume maintenance. 5 key findings →
Design: cross-sectional Participants: 4,322 Evidence: high
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Overall, memory worsened from age 30 years through the 90s. The HVa worsened gradually from age 30 years to the mid-60s and more steeply beyond that age. 5 key findings →
Design: cross-sectional Participants: 1,246 Evidence: low
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This study suggests that early tau deposition may follow multiple trajectories during preclinical AD and may involve several cortical regions. 3 key findings →
Design: cross-sectional Participants: 447 Evidence: moderate
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Disease-modifying therapies for Alzheimer's disease (AD) are likely to be most beneficial when initiated in the presymptomatic phase. 2 key findings →
Design: cross-sectional Participants: 567 Evidence: moderate
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Of 18 293 participants included in the parent study, scan images were available for 10 774 (59%), of which Centiloids were successfully calculated for 10 361 (96%). 1 key finding →
Design: cross-sectional Participants: 294 Evidence: low
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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 32,180 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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.
1,045 records (3.2% of the library) are not peer-reviewed — 966 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
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