28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.
Of a total 912 participants, there were 499 males (54.7%) and 413 females (45.3%), and the mean (SD) age was 71.1 (8.49) years. 5 key findings →
Design: cohort Participants: 912 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
Furthermore, plasma p-tau231 was significantly increased in amyloid-β PET quartiles 2-4, whereas CSF p-tau217 and plasma p-tau181 increased only at quartiles 3-4 and 4, respectively. 2 key findings →
Participants: 588 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
In this case-control study, blood biomarkers indicative of AD pathology demonstrated different dynamics of change after cardiac arrest. 5 key findings →
Design: case-control study Participants: 80 Evidence: high
Full summary, score breakdown and related studies → Original source Free full text
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
Full summary, score breakdown and related studies → Original source Free full text
Recently, conceptual systems for the in vivo staging of Alzheimer's disease (AD) using fluid biomarkers have been suggested. 4 key findings →
Participants: 219 Evidence: moderate
Full summary, score breakdown and related studies → Original source
P-tau181 detected AD at MCI and dementia stages and was strongly associated with cognitive decline and gray matter loss. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Elecsys-derived CSF biomarkers detect AD neuropathologic changes with very high discriminative accuracy in vivo. 2 key findings →
Participants: 27 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
N-p-tau217 and N-p-tau181 could improve diagnostic accuracy in prodromal-AD and clinical trial recruitment as both identify Aβ pathophysiology and differentiate early MCI-AD better than Mid-p-tau181. 2 key findings →
Participants: 503 Evidence: low
Full summary, score breakdown and related studies → Original source
After analytical validation, the diagnostic performance of these biomarkers was evaluated in CSF and compared with the Innotest total tau (and as proof of concept, with N-p-tau181 and N-p-tau217) in three clinical cohorts (n = 342 total). 5 key findings →
Participants: 342 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Well-authenticated biomarkers can provide critical insights into the biological basis of Alzheimer disease (AD) to enable timely and accurate diagnosis, estimate future burden and support therapeutic trials. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Blood phosphorylated tau (p-tau) biomarkers, at differing sites, demonstrate high accuracy to detect Alzheimer's disease (AD). 2 key findings →
Participants: 214 Evidence: low
Full summary, score breakdown and related studies → Original source
BV estimates for AD plasma biomarkers can potentially refine their clinical and research interpretation. 5 key findings →
Participants: 20 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers related to amyloid, tau, and neurodegeneration (ATN) show great promise for identifying these pathological features of Alzheimer's Disease (AD) as shown by recent clinical studies and selected autopsy studies. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
All CSF p-tau biomarkers were accurate predictors of cognitive impairment but CSF p-tau217 demonstrated the largest fold-changes in AD patients in comparison to non-AD dementias and cognitively unimpaired individuals. 3 key findings →
Participants: 171 Evidence: low
Full summary, score breakdown and related studies → Original source
Clinical trials testing tau-targeting therapies may benefit from using fluid biomarkers to recruit individuals at risk of tau aggregation. 1 key finding →
Participants: 163 Evidence: low
Full summary, score breakdown and related studies → Original source
Only increased serum NfL concentrations and decreased hippocampal volume was observed in cognitively unimpaired APOEε4 homozygotes compared to non-carriers. 5 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
Only Aβ burden measured by PET, but not markers of neuroinflammation, differed among cognitively unimpaired elderly with different APOE ε4 gene dose. 3 key findings →
Participants: 19 Evidence: low
Full summary, score breakdown and related studies → Original source
The same tube type should be used in research studies on blood biomarkers. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Understanding how plasma tau biomarkers are influenced by co-pathologies and comorbidities is crucial for their accurate implementation. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source Free full text
Our data suggest that AD-related biomarkers are altered by food intake. 2 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.
1,034 records (3.7% 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 →