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Find studies

Showing 1–25 of 128 studies in Brain scans and imaging · tagged Biomarkers (page 1 of 6) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

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

What “Brain scans and imaging” covers

Brain scans and imaging — MRI, PET and other scans: what they show, how early, and how reliably.

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.

Plasma pTau217R matched CSF eMTBR-tau243 and outperformed MTBR-tau243. 5 key findings →

Participants: 242 Evidence: low

CSF biomarkers of neuroinflammation and cerebrovascular dysfunction in early Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 73 out of 100. Neurology 2018-07-27

Neuroinflammation and cerebrovascular dysfunction are early events occurring already at presymptomatic stages of AD and contribute to disease progression. 5 key findings →

Design: longitudinal study Participants: 508 Evidence: moderate

The Alzheimer's disease neuroimaging initiative (ADNI): MRI methods

✓ Peer-reviewed alzhub usefulness score 72 out of 100. Journal of Magnetic Resonance Imaging 2008-02-26

The Alzheimer's Disease Neuroimaging Initiative (ADNI) is a longitudinal multisite observational study of healthy elders, mild cognitive impairment (MCI), and Alzheimer's disease. 5 key findings →

Design: longitudinal study Evidence: moderate

Although studies in animal models suggest that TREM2 is protective against Alzheimer's pathology, its effect on tau pathology and its potential beneficial role in people with Alzheimer's disease is still unclear. 4 key findings →

Design: longitudinal study Participants: 155 Evidence: moderate

Disease staging of Alzheimer's disease using a CSF-based biomarker model

✓ Peer-reviewed alzhub usefulness score 69 out of 100. Nature aging 2024-03-21

Biological staging of individuals with Alzheimer's disease (AD) may improve diagnostic and prognostic workup of dementia in clinical practice and the design of clinical trials. 4 key findings →

Design: longitudinal study Participants: 426 Evidence: moderate

The very mildest symptomatic stage of AD exhibits the same CSF biomarker phenotype as more advanced AD. 1 key finding →

Design: longitudinal study Participants: 139 Evidence: moderate

Longitudinal neuroimaging biomarkers differ across Alzheimer’s disease phenotypes

✓ Peer-reviewed alzhub usefulness score 67 out of 100. Brain 2020-04-29

Principal component analysis identified patterns of variation in baseline and longitudinal measures of tau uptake and volume that were significantly different across phenotypes. 2 key findings →

Design: longitudinal study Participants: 57 Evidence: moderate

In the Asan cohort, after adjusting for age and sex, p-tau181 (AUC = 0.854) or APOE ε4 status (AUC = 0.769) distinguished Aβ status with high accuracy. 5 key findings →

Design: cohort study Evidence: moderate

White matter hyperintensities and CSF Alzheimer disease biomarkers in preclinical Alzheimer disease

✓ Peer-reviewed alzhub usefulness score 65 out of 100. Neurology 2019-12-30

These results suggest that WMH primarily affect the risk of progression when CSF measures of neurodegeneration or neuronal injury (as reflected by t-tau) are low. 5 key findings →

Design: longitudinal study Participants: 274 Evidence: moderate

Amyloid imaging and CSF biomarkers in predicting cognitive impairment up to 7.5 years later

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Neurology 2013-04-10

Abnormal levels of all biomarkers were associated with faster time to cognitive impairment, and some participants with abnormal biomarker levels remained cognitively normal for up to 6.6 years. 2 key findings →

Design: longitudinal study Participants: 201 Evidence: moderate

Imaging and cerebrospinal fluid biomarkers in early preclinical alzheimer disease

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Annals of neurology 2016-07-25

CSF Aβ42 levels are tightly coupled with cortical amyloid load in the earliest stages of preclinical AD, and begin to decrease dramatically prior to the point when an abnormal threshold of cortical accumulation is detected with amyloid imaging. 1 key finding →

Design: longitudinal study Participants: 164 Evidence: moderate

Three- and 1-year progression risks were 86% (95% CI, 71%-95%) and 27% (95% CI, 17%-41%) when MRI results were abnormal, 82% (95% CI, 73%-89%) and 26% (95% CI, 20%-33%) when CSF test results were abnormal, and 89% (95% CI, 79%-95%) and 26% (95% CI, 18%-36%) when the results of both tests were abnormal. 4 key findings →

Design: longitudinal study Participants: 525 Evidence: moderate

MRI and CSF biomarkers in normal, MCI, and AD subjects: predicting future clinical change

✓ Peer-reviewed alzhub usefulness score 61 out of 100. Neurology 2009-07-01

MRI and CSF provide complimentary predictive information about time to conversion from amnestic mild cognitive impairment to Alzheimer disease and combination of the 2 provides better prediction than either source alone. 3 key findings →

Participants: 399 Evidence: low

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

Longitudinal change in CSF biomarkers in autosomal-dominant Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Science translational medicine 2014-03-01

Clinicopathological evidence suggests that the pathology of Alzheimer's disease (AD) begins many years before the appearance of cognitive symptoms. 3 key findings →

Design: cross-sectional Evidence: moderate

We found no significant correlation between CSF biomarkers and cognitive scores in any of the 3 clinical groups individually. 2 key findings →

Design: cross-sectional Participants: 399 Evidence: low

Physical activity attenuates age-related biomarker alterations in preclinical AD

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Neurology 2014-10-08

In a middle-aged, at-risk cohort, a physically active lifestyle is associated with an attenuation of the deleterious influence of age on key biomarkers of AD pathophysiology. 3 key findings →

Design: cross-sectional Participants: 186 Evidence: high

Association of Microglial Activation With Spontaneous ARIA-E and CSF Levels of Anti-Aβ Autoantibodies

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Neurology 2022-08-08

ARIA-E can also occur spontaneously in cerebral amyloid angiopathy-related inflammation (CAA-ri), a rare autoimmune encephalopathy associated with increased CSF levels of anti-Aβ autoantibodies. 5 key findings →

Design: longitudinal study Evidence: moderate

CSF and amyloid PET measurements of Aβ were consistent in the majority of subjects in the cross-sectional and longitudinal populations. 2 key findings →

Design: cross-sectional Participants: 374 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 27,380 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 27,380 records, built mostly from automated pulls of Europe PMC (60.6% of the library) and OpenAlex (18.6%), 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.

1,032 records (3.8% 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