30,580 Alzheimer's and dementia studies in plain English, each scored out of 100.
Plasma %p-tau217WashU had the highest performance, with significantly higher AUCs than all the immunoassays (Pdiff < 0.007). 5 key findings →
Design: cohort Participants: 998 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Plasma p-tau217 and tau positron emission tomography (PET) are strong prognostic biomarkers in Alzheimer's disease (AD), but their relative performance in predicting future cognitive decline among cognitively unimpaired (CU) individuals is unclear. 2 key findings →
Design: cohort Participants: 1,474 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Among 171 Aβ-positive CU participants included in the main analyses, 119 (mean [SD] age, 73.0 [5.4] years; 60.5% female) were from the BioFINDER-1 study, and 52 (mean [SD] age, 64.4 [4.6] years; 65.4% female) were from the WRAP study. 2 key findings →
Design: cohort study Participants: 564 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
In BioFINDER-2, the mean (SD) age was 65.7 (14.4) with 261 females (52.7%). 3 key findings →
Design: cohort Participants: 983 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
With the emergence of Alzheimer's disease (AD) disease-modifying therapies, identifying patients who could benefit from these treatments becomes critical. 1 key finding →
Participants: 1,422 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
However, because these biomarkers are strongly associated with the emergence of Aβ pathology, it is difficult to determine the contribution of insoluble tau aggregates to the plasma p-tau signal in blood. 5 key findings →
Design: longitudinal study Participants: 1,294 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Weight loss predicts AD CSF and PET biomarker results and may occur downstream to amyloid-β accumulation in preclinical AD, paralleling cognitive decline. 5 key findings →
Design: cohort study Participants: 2,743 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
Full summary, score breakdown and related studies → Original source Free full text
Although APOE4 is strongly associated with amyloid-β (Aβ), its relationship with tau accumulation is less understood. 5 key findings →
Design: cross-sectional Participants: 1,370 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Biological staging of individuals with Alzheimer's disease (AD) may improve diagnostic and prognostic workup of dementia in clinical practice and the design of clinical trials. 4 key findings →
Design: longitudinal study Participants: 426 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
P-tau/Aβ42 is sufficient for predicting progression in AD, with very high accuracy. 1 key finding →
Design: longitudinal study Participants: 1,983 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Aggregated insoluble tau is one of two defining features of Alzheimer's disease. 3 key findings →
Participants: 448 Evidence: low
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Several promising plasma biomarkers for Alzheimer's disease have been recently developed, but their neuropathological correlates have not yet been fully determined. 2 key findings →
Design: longitudinal study Participants: 105 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood biomarkers indicating elevated amyloid-β (Aβ) pathology in preclinical Alzheimer's disease are needed to facilitate the initial screening process of participants in disease-modifying trials. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Further analyses to determine clinical utility are warranted. 2 key findings →
Participants: 1,890 Evidence: low
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Insomnia in cognitively unimpaired adults at increased risk for AD is associated to poorer performance in some executive functions and volume changes in cortical and subcortical gray matter, including key areas involved in Alzheimer's disease, as well as decreased white matter diffusivity. 4 key findings →
Design: cross-sectional Participants: 366 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
The aim of this study was to evaluate longitudinal associations of multimodal core 1 AD biomarkers with cognition in a cognitively unimpaired (CU) population at increased risk of AD dementia. 4 key findings →
Design: longitudinal study Participants: 350 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
There are biologically meaningful Aβ-downstream effects in individuals with a low burden of Aβ pathology, while structural and functional changes are still subtle or absent. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF synaptic biomarkers increase in the early preclinical stages of the Alzheimer continuum even when a low burden of Aβ pathology is present, and they differ in their association with age, sex, APOE ε4 , and markers of neurodegeneration. 4 key findings →
Design: cross-sectional Evidence: moderate
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We analyzed data from 462 ADNI participants without dementia who underwent Aβ ([ 18 F]florbetapir or [ 18 F]florbetaben) and tau ([ 18 F]flortaucipir) PET, structural MRI, and cognitive testing. 4 key findings →
Design: cross-sectional Participants: 156 Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Disease staging, whereby the spatial extent and load of brain pathology are used to estimate the severity of Alzheimer disease (AD), is pivotal to the gold-standard neuropathological diagnosis of AD. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
In Alzheimer's disease (AD), tau phosphorylation in the brain and its subsequent release into cerebrospinal fluid (CSF) and blood is a dynamic process that changes during disease evolution. 4 key findings →
Evidence: low
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 30,580 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 →
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