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Find studies

Showing 851–875 of 3,083 studies · tagged Biomarkers (page 35 of 124) · 27,780 in the whole library · How the 0–100 score works

Download bibliography of the first 500 of these studies, in this order: BibTeX (.bib) · RIS (.ris)

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

A note on reading research. One study is rarely the final word.

We try to note the size of a study, whether it was in humans or animals, and how early-stage the finding is. If a summary here doesn't make that clear, treat it with extra caution and check the original source.

The combination of CSF biomarkers linked to different aspects of neurodegeneration, such as FABP3, α-syn, and AD biomarkers, improves the biochemical characterization of AD and Lewy body disorders. 4 key findings →

Participants: 48 Evidence: moderate

Plasma p-tau217 demonstrated better performance in the identification of AD pathology and clinical phenotypes in comparison with other variants of p-tau in a memory clinic cohort. 5 key findings →

Participants: 114 Evidence: moderate

The dynamics of plasma biomarkers across the Alzheimer's continuum

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Alzheimer's research & therapy 2023-02-08

This study is the first to delineate the trajectories of plasma biomarkers throughout the Alzheimer's continuum in the Chinese population, providing important implications for future trials targeting plasma GFAP to facilitate AD prevention and treatment. 3 key findings →

Participants: 206 Evidence: low

This study provides a systematic framework for selection of assay-specific cutpoints for clinical use of plasma p-tau217 for determination of amyloid status. 4 key findings →

Participants: 427 Evidence: low

Blood-based biomarkers are highly associated with amyloid PET/CSF results in diverse populations enrolled at clinical trial sites. 3 key findings →

Participants: 417 Evidence: low

Failures in Alzheimer's disease (AD) drug trials highlight the need to further explore disease mechanisms and alterations of biomarkers during the development of AD. 3 key findings →

Design: cross-sectional Participants: 377 Evidence: low

A Review of Fluid Biomarkers for Alzheimer's Disease: Moving from CSF to Blood

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Neurology and therapy 2017-07-21

A set of core cerebrospinal fluid (CSF) biomarkers for Alzheimer's disease (AD) includes total tau (T-tau), phosphorylated tau (P-tau) and β-amyloid 42 (Aβ42). 1 key finding →

Design: longitudinal study Evidence: moderate

MPP-Aβ might be one of the potential blood biomarkers for the prediction of PiB-PET positivity in the brain. 2 key findings →

Design: cross-sectional Participants: 353 Evidence: low

Unique AD-inflammatory biomarker correlations in a community-based cohort reveal a new avenue for utilizing plasma-based biomarkers in the assessment of AD and related dementias. 2 key findings →

Participants: 837 Evidence: moderate

A MPT model of the MST can detect individuals with AD prior to cognitive decline, making it a potentially useful tool for screening and monitoring older adults during the asymptomatic phase of AD. 1 key finding →

Participants: 200 Evidence: low

To date, the development of disease-modifying therapies for Alzheimer's disease (AD) has largely focused on the removal of amyloid beta Aβ fragments from the CNS. 4 key findings →

Participants: 59 Evidence: moderate

In addition to an overview of the results, we briefly outline the methods applied to the concept of resting-state functional connectivity. 4 key findings →

Design: longitudinal study Evidence: moderate

Plasma phosphorylated tau 217 and amyloid‑β 42/40 for amyloid risk in subgroups

✓ Peer-reviewed alzhub usefulness score 57 out of 100. Alzheimer's research & therapy 2025-08-07

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

Among 163 patients (mean age 69.3 ± 7.4 years, 52% female), plasma p-tau217 distinguished A+ from A- individuals (area under the curve [AUC] 0.90, 81% sensitivity, 91% specificity). 4 key findings →

Participants: 163 Evidence: low

P-tau217, p-tau231, p-tau181, α-syn, NfL, and GFAP levels were elevated in patients with NIID compared with HCs; p-tau species and GFAP were also upregulated in preNIID. 5 key findings →

Participants: 87 Evidence: low

Alzheimer's disease (AD), the most common age-dependent neurodegenerative disorder, is characterized neuropathologically by extracellular Aβ plaques and intracellular tau neurofibrillary tangles. 1 key finding →

Design: longitudinal study Evidence: moderate

Recent studies have demonstrated the high analytical and diagnostic performance of plasma p-tau217 using well-defined cohorts. 2 key findings →

Participants: 276 Evidence: low

Among 6437 participants screened, with non-Hispanic (NH) White as the reference group, odds ratios of plasma ineligibility were 2.88 (95% confidence interval [CI]: 1.40-6.96) for Hispanic Black, 1.60 (95% CI: 1.33-1.92) for Hispanic White, 2.10 (95% CI: 1.37-3.38) for NH Asian, and 1.59 (95% CI: 1.27-2.0) for NH Black participants. 3 key findings →

Participants: 6,437 Evidence: low

Higher plasma p-tau181 level was associated with worse memory, executive functioning, and language abilities, and greater informant-reported SCD. 5 key findings →

Participants: 1,185 Evidence: low

From across this tag

10 of the 3,069 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.

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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 →

Newest studies, as a dated timeline →    Atom feed