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Find studies

Showing 626–650 of 3,336 studies · tagged Biomarkers (page 26 of 134) · 28,180 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.

Except for αSyn, the additional biomarkers did not differentiate PD and HC, and none showed longitudinal differences, but most markers predict cognitive decline in PD during follow-up. 3 key findings →

Design: longitudinal study Evidence: moderate

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

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

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

Greater MVPA (β = -0.107; p = 0.013) and CRF (β = -0.114; p = 0.027) were associated with lower NfL, but not Aβ PET, p-tau217, Aβ1-42/1-40, or GFAP. 4 key findings →

Participants: 648 Evidence: moderate

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

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

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

Plasma NfL, GFAP, and pTau181 in patients with isolated REM sleep behavior disorder

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Sleep 2025-12-11

The study included 44 iRBD patients (81.8% males, mean age 71.0 ± 6.4 years), 55 HC (66.3% males, mean age 69.1 ± 5.5 years), and 28 AD patients (82.1% males, mean age of 70.4 ± 6.7 years). iRBD patients showed significantly higher plasma NfL and GFAP levels and similar pTau181 levels compared to HC. 5 key findings →

Design: cross-sectional Participants: 44 Evidence: low

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

In vitro studies of autosomal dominant Alzheimer's disease implicate longer amyloid-β peptides in disease pathogenesis; however, less is known about the behaviour of these mutations in vivo. 2 key findings →

Design: cohort study Evidence: moderate

Lumipulse and IP-MS Aβ42/40 exhibited the highest diagnostic accuracy for detecting an abnormal amyloid-PET (areas under the curve [AUCs] of 0.81 and 0.84, respectively). 5 key findings →

Participants: 179 Evidence: low

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

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

Characterization of Alzheimer's tau biomarker discordance using plasma, CSF, and PET

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Alzheimer's research & therapy 2021-05-04

Across different tau biomarker groups, the proportion of participants with a discordant profile varied (plasma+/CSF- 15.6%, plasma-/CSF+ 15.3%, plasma+/PET- 22.4%, and plasma-/PET+ 6.1%). 5 key findings →

Design: longitudinal study Evidence: moderate

This study directly compared four different commercial/lab p-tau217 blood tests (Lumipulse, ALZpath, Johnson & Johnson, and NULISA) in 344 people from two community cohorts, most of whom were cognitively normal or had only mild changes. 4 key findings →

Design: cross-sectional Participants: 344 Evidence: moderate

It was not possible to demonstrate significant differences on the co-primary clinical endpoints (ADAS-cog 11 and ADCS-ADL 23 ) at 52 weeks due to symptomatic activity in the control arm. 5 key findings →

Design: phase-3-trial Participants: 598 Evidence: null result

From across this tag

10 of the 3,322 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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