52/100
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
Research
31,380 Alzheimer's and dementia studies in plain English, each scored out of 100.
In patients with a discrepancy between CSF p-tau181 and CSF Aβ42, the assessment of Aβ 42/40 ratio led to a reliable biological conclusion in over 50% of cases that agreed with a clinician's diagnosis. 1 key finding →
Participants: 367 Evidence: low
Full summary, score breakdown and related studies → Original source
Studies on markers of inflammation in subjects with mild cognitive impairment or AD dementia provided inconsistent results. 5 key findings →
Design: cross-sectional Participants: 48 Evidence: low
Full summary, score breakdown and related studies → Original source
We examined whether plasma p-tau181 and p-tau217 are specific biomarkers of pathologically confirmed Alzheimer's disease (AD). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
While cerebrospinal fluid (CSF) biomarkers are of use in the prediction and diagnosis of Alzheimer's disease our understanding of the background effects of age and the ApoE genotype is limited. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 and p-tau217/Aβ1-42 are effective diagnostic tools. 4 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
CSF-to-plasma transition will open new avenues for molecular phenotyping of Alzheimer's disease (AD). 5 key findings →
Participants: 173 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Low or decreasing plasma Aβ42 during the follow-up is associated with cognitive decline. 2 key findings →
Participants: 269 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Alzheimer's disease (AD) is currently incurable, but there is general agreement that a minimally invasive blood biomarker for screening in preclinical stages would be crucial for future therapy. 5 key findings →
Design: cross-sectional Evidence: moderate
Full summary, score breakdown and related studies → Original source
Up to four freeze-thaw cycles do not influence single molecule array blood biomarkers of neurofilament light chain, total tau, or Aβ 42 , with at most minor reductions in Aβ 40 . 2 key findings →
Participants: 12 Evidence: low
Full summary, score breakdown and related studies → Original source
Increasingly, clinical trials for Alzheimer's disease (AD) are being conducted earlier in the disease phase and with biomarker confirmation using in vivo amyloid PET imaging or CSF tau and Aβ measures to quantify pathology. 1 key finding →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Highly sensitive and specific plasma biomarkers for Alzheimer's disease (AD) have the potential to improve diagnostic accuracy in the clinic and facilitate research studies including enrollment in prevention and treatment trials. 1 key finding →
Participants: 36 Evidence: moderate
Full summary, score breakdown and related studies → Original source
An 8-plex version of an isobaric reagent for the quantitation of proteins using shotgun methods is presented. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Elevated CSF p-Tau181 and NfL levels were associated with greater decline in memory and executive function. 5 key findings →
Participants: 136 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
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
In single predictor models, p-tau231 (AUC = 0.87, p = 0.005) and GFAP (AUC = 0.87, p = 0.01) were associated with amyloid positivity, and p-tau231 remained significant in all multi-predictor models (p-values < 0.02). 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Carriers had higher plasma p-tau217 levels than non-carriers. 5 key findings →
Participants: 24 Evidence: low
Full summary, score breakdown and related studies → Original source
Early imaging-based detection of acute ischemic stroke (AIS) has improved in the era of reperfusion therapy. 1 key finding →
Participants: 193 Evidence: low
Full summary, score breakdown and related studies → Original source
52/100
Plasma A+/T + individuals showed the highest levels of astrocyte reactivity, Aβ plaque, tau tangle, and axonal degeneration, and the lowest hippocampal volume and temporal-metaROI cortical thickness. 5 key findings →
Participants: 470 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
Heritability estimates were 16% for Aβ42/40, 42% for NfL, and 60% for GFAP. 5 key findings →
Evidence: low
Full summary, score breakdown and related studies → Original source
Specific plasma biomarker combinations predicted amyloid burden in the precuneus, tau in the entorhinal cortex, hippocampal atrophy, and memory decline. 3 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
Brain amyloidosis differentiated several measures, especially EDTA plasma pTa u 181 A β 42 ( d = 1.29). 4 key findings →
Participants: 38 Evidence: low
Full summary, score breakdown and related studies → Original source
Plasma AB42/40 had the highest AUC (0.833, 95% C.I. 0.767-0.899) at a cut-point of 0.0706 for discriminating between the two cerebral amyloid groups (sensitivity 76%, specificity 78.5%). 5 key findings →
Design: cross-sectional Evidence: low
Full summary, score breakdown and related studies → Original source
While the biomarkers available for Alzheimer's disease are continually expanding, including clinically approved blood tests, not all of the relationships between various biomarkers have been fully elucidated. 2 key findings →
Evidence: moderate
Full summary, score breakdown and related studies → Original source
From across this tag
9 of the 698 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 9. The same 9 appear here every time.
- Association of plasma p-tau and p-tau/Aβ ratio with Alzheimer's pathology
- Plasma biomarkers and incident clinical stage progression in the specialized memory clinic: a longitudinal study
- Plasma neurofilament light links mortality to neuroaxonal injury beyond clinical decline and Alzheimer disease plasma biomarkers: a multi-cohort study of oldest old individuals
- Symptom-Guided Blood Biomarker Testing for Alzheimer's Disease
- Plasma-derived biomarkers of Alzheimer's disease and neuropsychiatric symptoms: A community-based study
- Neuropsychological and behavioural correlates of CSF biomarkers in dementia
- Novel Biomarkers for Alzheimer's Disease: Plasma Neurofilament Light and Cerebrospinal Fluid
- Brain-Derived pTau217 and Plasma Proteomic Profiles Across Cognitive and Dementia Groups in Congolese Older Adults
- Protein fibril length in cerebrospinal fluid is increased in Alzheimer's disease
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