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Find studies

Showing 2,726–2,744 of 2,744 studies in Biomarkers (page 110 of 110) · 28,580 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.

What “Biomarkers” covers

Biomarkers — Measurable signals in blood, brain scans or spinal fluid that can indicate Alzheimer's changes.

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.

Epigenetic Clock Trajectories and Brain Health in Midlife

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-18

Middle-aged adults with faster 15-year epigenetic aging trajectories demonstrated worse cognitive performance, whereas those with slower biological aging trajectories exhibited cognitive resilience and more favorable AD biomarker profiles. 5 key findings →

Participants: 2,833 Evidence: low

Plasma metabolomic profiling of frailty in older adults at risk of dementia

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-08

Frailty index was associated with carboxylic acids and derivatives, fatty acyls and organooxygen compounds across multiple clusters, and a large number of lipids were linked to frailty score, potentially implicating dysregulation of energy metabolism in the pathophysiology of frailty and forming a panel of predictive biomarkers of at risk patients. 3 key findings →

Participants: 118 Evidence: low

A New Frontier in CWD Detection: Antemortem Plasma Biomarkers and Behavioral Profiling in Transgenic Mouse Models

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-08-10

Chronic Wasting Disease (CWD) is a fatal transmissible spongiform encephalopathy (TSE) that is confined to cervids (deer, moose, elk, and reindeer) but shares key properties with human neurodegenerative conditions such as Alzheimer’s, Parkinson’s, Huntington’s disease and frontal-temporal dementia. 2 key findings →

Evidence: low

All three frameworks recognized biologically coherent AD-related signal despite differences in training cohort and assay methodology. 1 key finding →

Participants: 472 Evidence: moderate

Association of total and brain-derived Alzheimer’s disease plasma biomarkers with brain amyloid deposition in a community-based sample

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-07-31

Bidirectional stepwise linear regression analysis was performed to identify plasma biomarkers associated with brain Aβ deposition. 5 key findings →

Design: cohort study Participants: 541 Evidence: moderate

Effect of prior traumatic brain injury on Alzheimer’s disease blood biomarkers in Vietnam Veterans

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-01-15

In this cross-sectional study (n=272), plasma pTau217/Aβ42 ratio test accuracy was 90% in Veterans without TBI history, but was significantly lower (63-78% accuracy) in Veterans with TBI history, with lowest accuracy in those with greater TBI severity. 5 key findings →

Design: cohort study Participants: 93 Evidence: moderate

Vasomechanic treatment increases efflux of human brain proteins

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-01-23

An age-related decline in vasodilation mediated by neurovascular nitric oxide (NO) and vasoconstriction driven by the Piezo1 receptor precede the aggregation of soluble brain proteins such as amyloid-β (Aβ), which then causes further disruption of brain solute homeostasis, ultimately leading to neurodegeneration in Alzheimer’s disease. 1 key finding →

Participants: 29 Evidence: low

Proteomic biomarkers of cognitive function, APOE ε4 status, and dementia in Generation Scotland

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-01-29

Untargeted mass spectrometry remains underutilised for blood-based biomarker discovery in dementia research from large cohorts, where affinity-based approaches dominate. 3 key findings →

Participants: 14,258 Evidence: low

ATN Classification and Machine-Learned Plasma Biomarker Phenotypes Reveal Distinct Alzheimer’s Pathology in a Population-Based Cohort

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-01-06

The analytic sample included 4,465 individuals (mean age 69.7±10.4 years; 58.7% female; 75.8% non-Hispanic White). 4 key findings →

Design: longitudinal study Participants: 51 Evidence: moderate

a Structured abstract BACKGROUND Over the past couple of decades, the role of infections, as well as the involvement of the immune system, have been highlighted in the development of dementia. 3 key findings →

Evidence: moderate

Multimodal latent composites are associated with cognition and Alzheimer’s disease dementia: a framework for systems-level brain health

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-02-23

Compared to the CN group, both MCI (β=−1.25, SE=0.19, p <.001) and AD dementia (β=−1.52, SE=0.16, p <.001) participants had lower Brain & Vascular Health composite scores. 3 key findings →

Participants: 197 Evidence: moderate

The current study was undertaken to unveil the protective effects of Luteolin, a natural flavonoid, against amyloid-beta (Aβ 1 - 42 )-induced neuroinflammation, amyloidogenesis, and synaptic dysfunction in mice. 5 key findings →

Evidence: low

This study is to examine if hydrogen-rich saline reduced amyloid beta (Abeta) induced neural inflammation, and learning and memory deficits in a rat model. 1 key finding →

Participants: 84 Evidence: low

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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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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