We analysed 461 participants from the DABNI and SPIN cohorts. 5 key findings →
Design: cross-sectional Participants: 461 Evidence: low
Full summary, score breakdown and related studies → Original source
Research
27,780 Alzheimer's and dementia studies in plain English, each scored out of 100.
We found that plasma p-tau217 was more associated with cognitive performance than p-tau181 and p-tau231 and that this relationship was particularly strong for memory scores (TRIAD: βp-tau217 = -0.53, βp-tau181 = -0.35 and βp-tau231 = -0.24; BioFINDER-2: βp-tau217 = -0.52, βp-tau181 = -0.24 and βp-tau231 = -0.29). 4 key findings →
Design: cross-sectional Participants: 103 Evidence: moderate
Full summary, score breakdown and related studies → Original source
(N = 558, mean age = 69.2 ± 8.8, 56.5% women) were diagnosed with AD (n = 274, considering dementia and MCI stages), frontotemporal dementia (FTD, n = 55), Lewy body disease (LBD, n = 40, considering MCI and dementia stages), other neurodegenerative diseases, n = 57 (e.g Supranuclear Palsy, Corticobasal syndrome), non-neurodegenerative cognitive impairment (NND, n = 79, e.g. vascular lesions, epilepsy or psychiatric disorders) or subjective cognitive impairment (SCI, n = 53). 4 key findings →
Design: cross-sectional Participants: 558 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Repetitive Head Impacts (RHI) in boxing may increase the risk for neuronal damage. 3 key findings →
Design: longitudinal study Participants: 15 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Deamidation products of blood albumin were significantly elevated in vascular dementia and frontotemporal dementia (P < 0.05), but less so in PD. 5 key findings →
Design: longitudinal study Participants: 140 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In the multivariable linear regression models, a doubling of serum molybdenum level was associated with 9.4% higher Aβ42/40 ratio (95% CI: 0.8, 18.6%; p = 0.03), and a doubling of serum cobalt level with 17.5% higher p-tau181 level (95% CI: 3.1, 33.8%; p = 0.02). 5 key findings →
Design: cross-sectional Participants: 194 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma p-tau217 levels measured using Lumipulse and Simoa assays were highly correlated (p < 0.001). 5 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
Patients with AD exhibit significantly higher CSF τ protein levels than healthy controls or patients with VaD in the Chinese population. 3 key findings →
Design: meta-analysis Evidence: high
Full summary, score breakdown and related studies → Original source
The NPTX2/p-tau ratio enhanced diagnostic performance of standalone NPTX2 and p-tau, particularly for DLB and FTLDrs (area under the curve [AUC]NPTX2/p-tau = 0.78-0.79 vs. AUCNPTX2 = 0.63-0.70 and AUCp-tau = 0.59-0.75), and was more strongly associated with cognition. 4 key findings →
Participants: 688 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated Tau 181 (pTau181) and CSF chitinase-3-like protein 1 (YKL-40) increased following semorinemab treatment in both studies. 5 key findings →
Design: clinical trial Evidence: low
Full summary, score breakdown and related studies → Original source
Niemann-Pick disease type C and Alzheimer's disease are distinct neurodegenerative disorders that share the presence of neurofibrillary tangle pathology. 4 key findings →
Design: cross-sectional Participants: 60 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Blood biomarkers indicating elevated amyloid-β (Aβ) pathology in preclinical Alzheimer's disease are needed to facilitate the initial screening process of participants in disease-modifying trials. 3 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
64/100
A combination of plasma p-tau181, NfL, and GFAP, but not Aβ 1-42/1-40 , might be useful to discriminate AD, FTD, and DLB. 1 key finding →
Participants: 160 Evidence: moderate
Full summary, score breakdown and related studies → Original source
PF and BF were significantly associated with increased likelihoods of dementia, Alzheimer's disease (AD), vascular dementia (VaD), and MCI. 5 key findings →
Design: cross-sectional Participants: 5,149 Evidence: low
Full summary, score breakdown and related studies → Original source
Higher plasma p-tau levels were associated with worse cognition at baseline and over time, with the strongest effect observed with p-tau217 in cognitively impaired individuals (β = -0.49, p < 0.001). 4 key findings →
Design: longitudinal study Evidence: moderate
Full summary, score breakdown and related studies → Original source
After adjusting for age, plasma NfL level was higher in subjects with DAT (65.98±84.96 pg/mL), compared to in subjects with SCD (16.90±2.54 pg/mL) or MCI (25.53±10.42 pg/mL, p=0.004). 5 key findings →
Design: longitudinal study Participants: 14 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Of 349 participants with available plasma data, 234 met inclusion criteria (31 controls, 141 in the training sample, and 62 in the validation sample). 5 key findings →
Design: cross-sectional Participants: 46 Evidence: low
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
Delirium is associated with cognitive decline and subsequent dementia, and rises in plasma total tau (tTau) and neurofilament light (NfL), providing links to Amyloid-Tau-Neurodegeneration (ATN) pathophysiology. 4 key findings →
Design: cohort study Participants: 54 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Participants were classified as hyposecretors (n = 22, median Aβ40 5,870.500 pg/mL, interquartile range [IQR] 1,431), normosecretors (n = 47, median Aβ40 10,817 pg/mL, IQR 3,622), and hypersecretors (n = 7, 19,767 pg/mL, IQR 3,088). 5 key findings →
Design: retrospective cohort Participants: 22 Evidence: moderate
Full summary, score breakdown and related studies → Original source
64/100
Family history (FH) of late-onset Alzheimer's disease (AD) is associated with changes in several cerebrospinal fluid (CSF) biomarkers in cognitively normal individuals. 2 key findings →
Design: longitudinal study Participants: 99 Evidence: moderate
Full summary, score breakdown and related studies → Original source
In subjects with biomarker-confirmed Alzheimer's pathology, high CSF ferritin (>6.2 ng/mL) was associated with accelerated depreciation of CSF Aβ1-42 (reporting increased plaque formation; p=0.0001). 5 key findings →
Design: longitudinal study Participants: 296 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Identifying which neuropsychological measures detect early cognitive changes associated with Alzheimer disease (AD), brain pathology would be helpful clinically for the diagnosis of early AD and for the design of clinical trials. 3 key findings →
Design: longitudinal study Participants: 233 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Intra- and inter-laboratory variability of cerebrospinal fluid (CSF) biomarker analyses remains an important issue. 1 key finding →
Design: longitudinal study Participants: 85 Evidence: moderate
Full summary, score breakdown and related studies → Original source
Plasma phosphorylated tau217 has been suggested as a core biomarker for establishing a biological Alzheimer's disease diagnosis. 2 key findings →
Design: cross-sectional Participants: 691 Evidence: low
Full summary, score breakdown and related studies → Original source
From across this tag
10 of the 710 studies in this tag, 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.
- Comparison of plasma and CSF biomarkers in predicting cognitive decline
- Combining a computerized cognitive test with serum biomarkers improves detection of early-onset neurodegenerative disorders
- A Decade of Blood Biomarkers for Alzheimer's Disease Research: An Evolving Field, Improving Study Designs, and the Challenge of Replication
- Diagnostic accuracy of automated Lumipulse plasma pTau-217 in Alzheimer's disease: a real-world study
- Proteomic studies of potential cerebrospinal fluid protein markers for Alzheimer's disease
- Potential Biomarkers in Cerebrospinal Fluid and Plasma for Dementia
- Amyloid-β misfolding as a plasma biomarker indicates risk for future clinical Alzheimer's disease in individuals with subjective cognitive decline
- A novel ultrasensitive assay for plasma p-tau217: Performance in individuals with subjective cognitive decline and early Alzheimer's disease
- Dynamics of plasma biomarkers in Down syndrome: the relative levels of Aβ42 decrease with age, whereas NT1 tau and NfL increase
- 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 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.
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 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 →