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Find studies

Showing 26–50 of 455 studies in Biomarkers · tagged Brain Scans (page 2 of 19) · 31,380 in the whole library · How the 0–100 score works

Download bibliography of these 455 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.

For all 4 phosphorylation sites assessed in CSF, p-tau was significantly more closely associated with amyloid-PET values than tau-PET values (p-tau181 difference, 13%; 95% CI, 3%-22%; P = .006; p-tau217 difference, 11%; 95% CI, 3%-20%; P = .003; p-tau231 difference, 15%; 95% CI, 5%-22%; P Conclusions and relevance Results of this cross-sectional study of 2 observational cohorts suggest that the p-tau abnormality as an early event in AD pathogenesis was associated with amyloid-β accumulation and highlights the need for careful interpretation of p-tau biomarkers in the context of the amyloid/tau/neurodegeneration, or A/T/(N), framework. 2 key findings →

Design: cross-sectional Participants: 609 Evidence: moderate

It is currently unclear whether plasma biomarkers can be used as independent prognostic tools to predict changes associated with early Alzheimer's disease. 4 key findings →

Design: longitudinal study Participants: 123 Evidence: moderate

In the precuneus, we observed an inverted U-shaped pattern of novelty-related activity across groups, with higher activity in SCD and MCI compared with HC, but not in patients with AD who showed relatively lower activity than MCI. 3 key findings →

Design: longitudinal study Participants: 499 Evidence: moderate

We demonstrated that higher amyloid burden as measured by both CSF amyloid beta 42/40 ratio and non-displaceable binding potential in the posterior cingulate cortex was associated with lower functional connectivity in the default mode network. 3 key findings →

Design: longitudinal study Participants: 173 Evidence: moderate

Plasma p-tau217 showed the strongest individual association with Aβ PET status (area under the curve [AUC], 0.85). 5 key findings →

Design: cohort study Participants: 1,407 Evidence: moderate

The A+P+T- group showed a slower rate of increase in tau-PET compared to the A+P+T+ group, primarily in neocortical regions. 4 key findings →

Design: longitudinal study Participants: 231 Evidence: moderate

Alzheimer's disease diagnostic accuracy by fluid and neuroimaging ATN framework

✓ Peer-reviewed alzhub usefulness score 71 out of 100. CNS neuroscience & therapeutics 2023-07-12

Our findings suggest that plasma, CSF, and neuroimaging biomarkers differ considerably within the ATN framework; the most accurate target biomarkers for diagnosing AD were the CSF-A, neuroimaging-T, and neuroimaging-N within each ATN modality. 4 key findings →

Design: longitudinal study Participants: 2,340 Evidence: moderate

These findings indicate that plasma pTau181, plasma pTau217 and amyloid-β PET convey overlapping information and therefore predict the dynamic phase of asymptomatic amyloid-β accumulation with comparable performances. 1 key finding →

Design: cohort study Participants: 75 Evidence: moderate

Analyses measured the associations between predictor variables and the memory score, and whether AT(N) biomarker profiles significantly improved prediction of memory z score rates of change beyond a model with clinical and genetic variables only. 3 key findings →

Design: cohort study Participants: 480 Evidence: moderate

These findings suggest that this blood biomarker test could allow for distinguishing individuals with brain amyloid-positive PET findings from individuals with amyloid-negative PET findings and serve as an aid for Alzheimer disease diagnosis. 4 key findings →

Design: cohort study Participants: 249 Evidence: moderate

We analyzed 1,240 MRIs from 473 patients (age: 69.2 ± 7.4 [range: 49-87]; 32.8% women). 2 key findings →

Design: cohort study Participants: 1,240 Evidence: moderate

Levels of plasma p-tau217 increased significantly in Aβ+ participants before showing significant deceleration (χ2 = 21.7; P Conclusions and relevance This study found that tau PET is valuable for both prognostic and real-time tracking of disease progression. 2 key findings →

Design: cohort Participants: 1,707 Evidence: moderate

Plasma p-tau217 may capture earlier Alzheimer's disease (AD)-related cognitive and brain atrophy hallmarks in females compared to males, possibly reflective of increased susceptibility to AD pathophysiology. 2 key findings →

Design: longitudinal study Participants: 163 Evidence: moderate

In TAP-TAU, we will investigate the added clinical value of tau-PET in a real-world clinical setting, including memory clinic patients with diagnostic uncertainty after routine work-up. 2 key findings →

Design: longitudinal study Participants: 300 Evidence: moderate

Multitracer model for staging cortical amyloid deposition using PET imaging

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Neurology 2020-07-16

SUVr abnormality was most frequently observed in cingulate, followed by orbitofrontal, precuneal, and insular cortices and then the associative, temporal, and occipital regions. 1 key finding →

Design: longitudinal study Participants: 867 Evidence: moderate

In a community-based cohort of 70-year olds, P-NfL was associated with both prevalent and incident CKD, while CSF and/or imaging measures did not differ by CKD status. 3 key findings →

Design: cohort study Participants: 744 Evidence: moderate

Presence on T2-weighted images of white matter hyperintensities (WMH) has been previously shown to be more commonly associated with GRN mutations rather than other forms of FTD. 5 key findings →

Design: longitudinal study Participants: 336 Evidence: moderate

Brain volume analyses included 622 participants (mean age ± SD: 70.9 ± 10.2) with an average of 3.3 MRI scans over 4.7 years. 5 key findings →

Design: longitudinal study Participants: 622 Evidence: moderate

The dynamics of biomarkers across the clinical spectrum of Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 67 out of 100. Alzheimer's research & therapy 2020-06-13

Despite the limited longitudinal data at the individual level and the high variability observed in such data, the study elucidates the link between the long asynchronous pathophysiological processes and the preclinical and clinical stages of AD. 2 key findings →

Design: longitudinal study Participants: 2,014 Evidence: moderate

Cognitive and neuropsychological scores differed significantly among the groups, with descending performance among CN>SCD>MCI>AD. 4 key findings →

Design: longitudinal study Participants: 128 Evidence: moderate

These data suggest that apoJ may have potential in the context of use (COU) of AD diagnostics, I-309 may be specifically useful in the COU of identifying individuals at greatest risk for progressing toward AD. 2 key findings →

Design: longitudinal study Participants: 14 Evidence: moderate

Remote Blood Biomarkers of Longitudinal Cognitive Outcomes in a Population Study

✓ Peer-reviewed alzhub usefulness score 66 out of 100. Annals of neurology 2020-09-29

Higher concentrations of serum biomarkers were associated with the development of clinical AD; especially, the time-specific associations were notable: t-tau 8 to 16 years, and Nf-L and GFAP 4 to 8 years prior to clinical AD. 3 key findings →

Design: longitudinal study Participants: 1,327 Evidence: moderate

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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 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