27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
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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The very mildest symptomatic stage of AD exhibits the same CSF biomarker phenotype as more advanced AD. 1 key finding →
Design: longitudinal study Participants: 139 Evidence: moderate
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Thinning in specific cortical areas known to be affected by Alzheimer disease (AD) is detectable in individuals with questionable AD dementia (QAD) and predicts conversion to mild AD dementia. 3 key findings →
Design: longitudinal study Participants: 49 Evidence: moderate
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See Li and Donohue (doi:10.1093/brain/awy089) for a scientific commentary on this article. 4 key findings →
Design: longitudinal study Participants: 338 Evidence: moderate
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Baseline CSF levels of NGRN in patients with AD (median level, 2381 pg/mL [interquartile range, 1651-3416 pg/mL]) were higher than in cognitively normal participants (median level, 1712 pg/mL [interquartile range, 1206-2724 pg/mL]) (P = .04). 3 key findings →
Design: longitudinal study Participants: 163 Evidence: moderate
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The temporal evolutions and relative orderings of Alzheimer disease biomarkers, including CSF amyloid-β42 (Aβ42), Aβ40, total tau (Tau) and phosphorylated tau181 (pTau181), standardized uptake value ratio (SUVR) from the molecular imaging of cerebral fibrillar amyloid-β with PET using the 11C-Pittsburgh Compound-B (PiB), MRI-based hippocampal volume and cortical thickness and cognition have been hypothesized but not yet fully tested with longitudinal data for all major biomarker modalities among cognitively normal individuals across the adult lifespan starting from 18 years. 4 key findings →
Design: longitudinal study Participants: 2,609 Evidence: moderate
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Among the 174 participants (81 men [46.6%]; 93 women [53.4%]; mean [SD] age, 65.7 [8.9] years), a proportion (14%-17%) of individuals with neurodegeneration alone (SNAP) later demonstrated Aβ+. 1 key finding →
Design: cohort study Participants: 174 Evidence: moderate
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The amyloid/tau/neurodegeneration (A/T/N) framework uses cerebrospinal fluid (CSF) levels of total tau (tTau) as a marker of neurodegeneration and CSF levels of phosphorylated tau 181 (pTau181) as a marker of tau tangles. 4 key findings →
Design: cohort study Participants: 465 Evidence: moderate
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Patients with DLB had an increased risk of mortality vs patients with AD (hazard ratio [HR] 1.88, 95% CI: 1.4 to 2.5). 3 key findings →
Design: longitudinal study Participants: 315 Evidence: moderate
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Aging with and without DAT is associated with weight loss; however, weight loss may accelerate before the diagnosis of DAT. 2 key findings →
Design: longitudinal study Participants: 449 Evidence: moderate
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Changes in functional connectivity in DLB indicate patterns of activation that are distinct from those seen in AD and may improve discrimination of DLB from AD and cognitively normal individuals. 3 key findings →
Design: longitudinal study Participants: 88 Evidence: moderate
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With the aging US population and increasing incidence of Alzheimer disease (AD), understanding factors contributing to driving cessation among older adults is crucial for clinicians. 4 key findings →
Design: longitudinal study Participants: 283 Evidence: moderate
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This study examined rates of dementia progression as ascertained by the Clinical Dementia Rating Sum of Boxes (CDR-SB) for symptomatic Alzheimer's disease (sAD), and assessed participant characteristics as predictors of CDR-SB progression. 3 key findings →
Design: longitudinal study Participants: 792 Evidence: moderate
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The lack of effective predictors of the rate of dementia progression extends to the very earliest stages of the disease, including what is often called MCI. 1 key finding →
Design: longitudinal study Participants: 289 Evidence: moderate
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Cognitive dysfunction, including dementia and delirium, is prevalent in geriatric emergency department (ED) patients, but often remains undetected. 4 key findings →
Design: cohort study Participants: 163 Evidence: moderate
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While prior work reliably demonstrates that the APOE ɛ4 allele has deleterious group level effects on Alzheimer disease pathology, the homogeneity of its influence across the lifespan and spatially in the brain remains unknown. 1 key finding →
Design: longitudinal study Evidence: moderate
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Preclinical AD as detected by PET PiB is not benign, as it is associated with progression to symptomatic AD. 4 key findings →
Design: cohort study Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid (CSF) levels of Abeta peptide 1-42 (Abeta 42), tau, and phosphorylated tau (ptau) are potential biomarkers of Alzheimer disease. 4 key findings →
Design: longitudinal study Participants: 49 Evidence: moderate
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Identifying high-risk populations is an important component of disease prevention strategies. 2 key findings →
Design: longitudinal study Participants: 100 Evidence: moderate
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The mean (SD) age at death was statistically significantly younger for participants who had AD with Lewy bodies (77.9 [9.5] years) than for participants who had AD without Lewy bodies (80.2 [11.1] years) (P = .01). 2 key findings →
Design: cohort study Evidence: moderate
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Measures of neuronal loss are likely good surrogates for clinical and radiological disease progression in Alzheimer disease (AD). 4 key findings →
Design: longitudinal study Participants: 23 Evidence: moderate
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In a longitudinal study of senile dementia and healthy aging, the occurrence of serious falls was examined in participants with senile dementia of the Alzheimer's type (SDAT) (n = 44) and in cognitively healthy elderly control participants (n = 56) over a 4-year period. 4 key findings →
Design: longitudinal study Participants: 44 Evidence: moderate
Full summary, score breakdown and related studies → Original source
This study provides longitudinal evidence for a decline in driving performance over time, primarily in early-stage DAT, and supports the need not only for driving assessments, but also for reevaluation of individuals with very mild and mild DAT. 3 key findings →
Design: longitudinal study Participants: 21 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Knight Alzheimer's Disease Research Center (ADRC) at Washington University (WU). 4 key findings →
Design: longitudinal study Participants: 118 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. 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 →