Plasma phosphorylated-tau217 (p-tau217) has been shown to be one of the most accurate diagnostic markers for Alzheimer's disease. 3 key findings →
Participants: 392 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
To improve clinical utility, a dual threshold approach was applied to maximize predictive values and positive likelihood ratios while minimizing the proportion of indeterminate results. 5 key findings →
Participants: 208 Evidence: low
Full summary, score breakdown and related studies → Original source
Among 191 participants (57 Black, 46 Hispanic White, 88 non-Hispanic White), age-adjusted plasma p-tau217 and p-tau217/Aβ42 performed similarly in detecting amyloid-positive individuals (≥ 25 Centiloids), regardless of race/ethnicity. 5 key findings →
Participants: 191 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 demonstrated the strongest discrimination of Core1 positivity (area under the curve [AUC] = 0.95) and showed the steepest increase with disease progression. 4 key findings →
Participants: 401 Evidence: low
Full summary, score breakdown and related studies → Original source
Amyloid status was determined by CSF in 347 patients (189 positive [54.5%]) and by PET imaging in 152 patients (66 positive [43.4%]). 4 key findings →
Participants: 499 Evidence: low
Full summary, score breakdown and related studies → Original source
61/100
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
BackgroundDiabetes has been linked to increased prevalence of dementia, but the link between diabetic retinopathy (DR) and Alzheimer's disease (AD) remains unclear. 4 key findings →
Design: cross-sectional Participants: 79 Evidence: low
Full summary, score breakdown and related studies → Original source
White matter hyperintensities (WMH) is mainly caused by cerebrovascular injury and may also increase the possibilities of progression to Alzheimer's disease. 2 key findings →
Design: cross-sectional Participants: 1,029 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Biomarkers were correlated with one another. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
The CSF A/T profiles included 49 A+/T+, 8 A+/T-, and 41 A-/T-. 5 key findings →
Design: cross-sectional Participants: 98 Evidence: low
Full summary, score breakdown and related studies → Original source
Of the 859 participants enrolled in this ongoing study, 20.6% self-identified as Black or African American. 5 key findings →
Participants: 859 Evidence: moderate
Full summary, score breakdown and related studies → Original source
A total of 337 participants were included: 136 ND, 77 PPD, and 124 Controls. 5 key findings →
Participants: 337 Evidence: low
Full summary, score breakdown and related studies → Original source
In a previous proteomic study, we identified the neurosecretory protein VGF (VGF) as a potential biomarker for dementia with Lewy bodies (DLB). 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Several plasma p-tau biomarkers can be used in a specialized memory clinic as a stand-alone biomarker to detect biologically-defined AD. 2 key findings →
Participants: 197 Evidence: low
Full summary, score breakdown and related studies → Original source
Our data suggest that measuring blood biomarkers related to AD pathology and neurodegeneration from DPS venous extends the utility of blood-based biomarkers to remote settings with simplified sampling conditions, storage, and logistics. 4 key findings →
Participants: 154 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Combinations of plasma and digital cognitive markers show promise for scalable diagnosis and prognosis of ADRD. 1 key finding →
Participants: 49 Evidence: low
Full summary, score breakdown and related studies → Original source
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
Both plasma p-tau217 assays were strongly associated with amyloid and tau PET. 1 key finding →
Participants: 294 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma amyloid-β (Aβ)42, phosphorylated tau (p-tau)181, and neurofilament light chain (NfL) are promising biomarkers of Alzheimer's disease (AD). 2 key findings →
Participants: 126 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Comparable diagnostic performances and strong correlations between serum versus plasma pairs suggest that p-tau analyses can be expanded to research cohorts and hospital systems that prefer serum to other blood matrices. 5 key findings →
Participants: 115 Evidence: moderate
Full summary, score breakdown and related studies → Original source
59/100
Amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) are two related currently incurable neurodegenerative diseases. 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Longitudinal multimodal biomarker studies reveal that the continuum of Alzheimer's disease (AD) includes a long latent phase, referred to as preclinical AD, which precedes the onset of symptoms by decades. 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
59/100
In this study, levels of total A(beta)x-40 and A(beta)x-42 were elevated early in dementia and levels of both peptides were strongly correlated with cognitive decline. 4 key findings →
Design: cross-sectional Participants: 16 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma biomarkers have emerged as promising less invasive alternatives for Alzheimer's disease (AD) detection. 2 key findings →
Participants: 53 Evidence: moderate
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 695 studies in this tag that have a study page, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 10. The same 10 appear here every time.
- Diagnostic Accuracy of Blood-Based Biomarker Panels: A Systematic Review
- The diagnostic and prognostic capabilities of plasma biomarkers in Alzheimer's disease
- Association of plasma glial fibrillary acidic protein (GFAP) with neuroimaging of Alzheimer's disease and vascular pathology
- Measurement of thirteen biological markers in CSF of patients with Alzheimer's disease and other dementias
- Csf p-tau181/tau ratio as biomarker for TDP pathology in frontotemporal dementia
- Genetic risk and plasma biomarkers of dementia with Lewy bodies in a Chinese population
- Cerebrospinal fluid biomarkers in Alzheimer's disease, vascular dementia and ischemic stroke patients: a critical analysis
- Novel CSF tau biomarkers can be used for disease staging of sporadic Alzheimer's disease
- Neurofilament protein in cerebrospinal fluid: a marker of white matter changes
- Plasma phosphorylated tau 217 and amyloid‑β 42/40 for amyloid risk in subgroups
Where “Free full text” comes from
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
How the 0–100 score works — and why some entries are capped
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.
- Journal tier up to 10 pts
- Journal's citation record up to 4 pts
- Study design up to 12 pts
- Strength of evidence up to 5 pts
- Peer-review validation up to 10 pts
- How recent up to 5 pts
- Sample size up to 4 pts
- Effect reported up to 3 pts
- Studied in people up to 3 pts
- Randomised / blinded up to 2 pts
- Times cited up to 7 pts
- Citations per year up to 5 pts
- Impact for its field and year up to 6 pts
- Cited by studies here up to 6 pts
- Still being cited up to 4 pts
- Senior author's track record up to 4 pts
- Institution's track record up to 3 pts
- Multi-centre collaboration up to 3 pts
- Indexed in PubMed up to 2 pts
- Free to read up to 2 pts
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 31,380 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.
What this library is — and isn't
This is a large sample of the Alzheimer's literature, not an exhaustive index of it. It holds 31,380 records, built mostly from automated pulls of Europe PMC (65.6% of the library) and OpenAlex (16.2%), 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.
1,048 records (3.3% of the library) are not peer-reviewed — 973 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 →
Newest studies, as a dated timeline → Atom feed Where this research is being discussed: events