27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
Hallucinations, delusions, and depression were more common in DLB than in AD and, in a subgroup with longitudinal follow-up, persistent hallucinations and NPSs were associated with lower p-tau181 and p-tau231 in DLB. 5 key findings →
Design: longitudinal study Participants: 222 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A blood biomarker-based staging system for Alzheimer's disease (AD) could improve the diagnosis, prognosis and identification of individuals most likely to benefit from specific therapies. 3 key findings →
Design: longitudinal study Participants: 689 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Mixed-effect models assessed rates of memory decline in relation to baseline plasma p-tau181, and whether plasma p-tau181 significantly predicted memory decline beyond widely available clinical and genetic data (age, sex, years of education, cardiovascular and metabolic conditions, and APOEε4 status). 5 key findings →
Design: longitudinal study Participants: 604 Evidence: moderate
Full summary, score breakdown and related studies → Original source
We included 400 middle-aged CU participants, of whom 135 (33.8%) were CSF Aβ-positive. 5 key findings →
Design: cross-sectional Participants: 400 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau biomarkers had a greater diagnostic performance and larger effect sizes compared to t-tau and Aβ42/40 assays in detecting Aβ pathology. 5 key findings →
Design: cross-sectional Participants: 197 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma GFAP discriminated AD dementia from normal cognition (adjusted mean difference = 0.90 standard deviation [SD]) and mild cognitive impairment (adjusted mean difference = 0.72 SD), and demonstrated superior discrimination compared to alternative plasma biomarkers. 4 key findings →
Design: cross-sectional Participants: 567 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Multiple proteinopathies commonly coexist in neurodegenerative diseases, making it essential to evaluate plasma biomarker performance in these complex diseases. 2 key findings →
Participants: 253 Evidence: moderate
Full summary, score breakdown and related studies → Original source
E280A carriers had higher p-tau231 levels than non-carriers (9.0 ± 7.4 vs. 5.2 ± 3.4 pg/mL, P < 0.001). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
NfL demonstrated fair to excellent accuracy in differentiating non-ACS from CU groups (area under the curve [AUC], 0.79 to 0.94). p-tau217 had the highest accuracy for identifying Aβ (AUC 0.94) and tau positron emission tomography status (AUC 0.91). 5 key findings →
Participants: 2,984 Evidence: low
Full summary, score breakdown and related studies → Original source
Aβ-independent factors included hemoglobin and estimated glomerular filtration rate (eGFR) for p-tau217 and hemoglobin, eGFR, and triiodothyronine (T3) for GFAP and NfL. 5 key findings →
Participants: 2,935 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In CU individuals from the development cohort, the combination of p-tau217 and Aβ42/40 significantly improved diagnostic accuracy (AUC: ALZpath 0.937 vs. 0.905, MSD 0.901 vs. 0.861; p < 0.05, DeLong test; 95% CIs) and model fit (AIC /BIC, p < 0.001) compared to p-tau217 alone. 5 key findings →
Participants: 1,545 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Baseline NfL and GFAP did not differ between patients with or without ARIA (ln[NfL] ECLIA 1.24 ± 0.38 pg/mL vs 1.25 ± 0.40 pg/mL, p = 0.77; ln[NfL] Simoa 2.87 ± 0.47 pg/mL vs 2.98 ± 0.40 pg/mL, p = 0.30, ln[GFAP] ECLIA 4.95 ± 0.36 pg/mL vs 4.88 ± 0.47 pg/mL, p = 0.69). 4 key findings →
Participants: 15 Evidence: low
Full summary, score breakdown and related studies → Original source
N-terminal p-tau was increased in CJD versus SCD (p < 0.0001) and correlated with total tau (t-tau) in the presence of AD and PART co-pathology (rho = 0.758-0.952, p ≤ 001). 5 key findings →
Participants: 29 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated-tau (p-tau) biomarkers show high performance as first-in-line tests in the evaluation of patients with cognitive symptoms and have also found utility in clinical trials for anti-amyloid drug therapies for Alzheimer's disease (AD). 2 key findings →
Participants: 317 Evidence: low
Full summary, score breakdown and related studies → Original source
Phosphorylated tau 181 (p-tau181), phosphorylated tau 231 (p-tau231), neurofilament light (NfL), and glial fibrillary acidic protein (GFAP) concentrations were unchanged both when stored at +4°C and +18°C. Amyloid-β 40 (Aβ40) and amyloid-β 42 (Aβ42) concentrations were stable for 24 h at +4°C but declined when stored at +18°C for longer than 6 h. This decline did not affect the Aβ42/Aβ40 ratio. 5 key findings →
Participants: 13 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers have shown promising performance in research cohorts in discriminating between different stages of Alzheimer's disease (AD). 2 key findings →
Participants: 75 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated tau at threonine-181 (P-tau181) demonstrates promise as an accessible blood-based biomarker specific to Alzheimer's Disease (AD), with levels recently demonstrating high predictive accuracy for AD-relevant pathology. 2 key findings →
Participants: 1,153 Evidence: low
Full summary, score breakdown and related studies → Original source
Worse overall and local LC-EC integrity, indicated by lower fractional anisotropy (FA) and higher mean diffusivity (MD), was related to elevated concentrations of plasma phosphorylated tau 181 (p-tau181), p-tau217, and glial fibrillary acidic protein (GFAP). 5 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Lower cerebrospinal fluid (CSF) ApoE, higher CSF p-tau181/amyloid-β (Aβ)42, and higher plasma p-tau231/Aβ42 were associated with higher variability of sleep midpoint, sleep duration, and/or activity count. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated tau (p-tau) and glial fibrillary acidic protein (GFAP) both reflect early changes in Alzheimer's disease (AD) pathology. 3 key findings →
Participants: 88 Evidence: low
Full summary, score breakdown and related studies → Original source
As plasma biomarkers like p-tau217 move towards clinical use in Alzheimer's disease (AD), it is important to understand how kidney function may influence their accuracy. 1 key finding →
Evidence: low
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is characterised by a long preclinical phase. 3 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 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 →