27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
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
Plasma P-tau181/Aβ42 ratio may be a noninvasive means of identifying AD with elevated brain amyloid in populations with concomitant CeVD. 3 key findings →
Participants: 43 Evidence: moderate
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-based biomarkers such as tau phosphorylated at threonine 181 (phosphorylated-tau181) represent an accessible, cost-effective and scalable approach for the in vivo detection of Alzheimer's disease pathophysiology. 5 key findings →
Participants: 103 Evidence: low
Full summary, score breakdown and related studies → Original source
Blood-based biomarkers may differentiate non-AD-related versus AD-related cognitive deficits. 5 key findings →
Participants: 648 Evidence: low
Full summary, score breakdown and related studies → Original source
Serum GFAP is increased in FTLD, correlates with cognition and GABAergic deficits, and thus shows promise as a biomarker of disease severity in FTLD. 3 key findings →
Design: cross-sectional Participants: 406 Evidence: moderate
Full summary, score breakdown and related studies → Original source
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
As the leading cause of dementia, Alzheimer's disease (AD) is a major burden on affected individuals, their families and caregivers, and healthcare systems. 1 key finding →
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
Increasing variation greatly impacted the performance of plasma Aβ42/40 in discriminating Aβ status. 1 key finding →
Participants: 50 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma p-tau231 showed more robust associations with PET biomarkers than p-tau181 in presymptomatic individuals. 1 key finding →
Participants: 129 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma tau phosphorylated at threonine 181 (p-tau181) predicts Alzheimer's disease (AD) pathology with high accuracy in the general population. 2 key findings →
Participants: 366 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
CSF tau368 concentration was not significantly different across the diagnostic groups, although a modest increase was observed in all groups as compared with healthy young individuals (all P < 0.01). 5 key findings →
Participants: 125 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Phosphorylated tau (p-tau) 217 is a promising blood biomarker for Alzheimer's disease (AD). 3 key findings →
Participants: 50 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Recent studies suggest that plasma phosphorylated tau181 (p-tau181) is a highly specific biomarker for Alzheimer's disease (AD)-related tau pathology. 4 key findings →
Participants: 818 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Cerebrospinal fluid analyses and neuroimaging can identify the underlying pathophysiology at the earliest stage of some neurodegenerative disorders, but do not have the scalability needed for population screening. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
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
Plasma and CSF p-tau 217 had equivalent diagnostic performance for biomarker-defined AD. 2 key findings →
Participants: 174 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
These results support plasma p-tau 181 for the detection of AD dementia and the use of blood-based biomarkers for optimal disease detection. 2 key findings →
Participants: 235 Evidence: low
Full summary, score breakdown and related studies → Original source
Comparing clinical stages, CSF PDGFRβ levels were increased at the MCI stage (Cohen's d = 0.55 [CI 95% 0.066, 1.0], P = 0.025) compared with NC. 3 key findings →
Participants: 23 Evidence: low
Full summary, score breakdown and related studies → Original source Free full text
Nighttime vasomotor symptoms may be a marker of women at risk of Alzheimer disease. 4 key findings →
Participants: 274 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 27,780 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 27,780 records, built mostly from automated pulls of Europe PMC (61.1% of the library) and OpenAlex (18.3%), 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 →