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Find studies

Showing 1–25 of 65 studies in Brain scans and imaging with an author at Mayo Clinic (US) (page 1 of 3) · 28,180 in the whole library · How the 0–100 score works

Download bibliography of these 65 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 “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.

We found a sequence to pathological changes, with rates of Aβ deposition in mutation carriers being significantly different from those in non-carriers first (across regions that showed a significant difference, at a mean of 18·9 years [SD 3·3] before expected onset), followed by hypometabolism (14·1 years [5·1] before expected onset), and lastly structural decline (4·7 years [4·2] before expected onset). 2 key findings →

Design: longitudinal study Participants: 346 Evidence: moderate

Sex Differences in Longitudinal Tau-PET in Preclinical Alzheimer Disease: A Meta-Analysis

✓ Peer-reviewed alzhub usefulness score 76 out of 100. JAMA neurology 2025-03-03

Mounting evidence in adults without AD indicates that females exhibit higher tau deposition than age-matched males, particularly in the setting of elevated β-amyloid (Aβ), but the evidence for sex differences in tau accumulation rates is inconclusive. 5 key findings →

Design: meta-analysis Participants: 1,376 Evidence: high

Association Between Elevated Brain Amyloid and Subsequent Cognitive Decline Among Cognitively Normal Persons

✓ Peer-reviewed alzhub usefulness score 73 out of 100. JAMA 2017-06-01

Among the 445 participants (243 with normal amyloid, 202 with elevated amyloid), mean (SD) age was 74.0 (5.9) years, mean education was 16.4 (2.7) years, and 52% were women. 2 key findings →

Design: longitudinal study Participants: 243 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

Midlife systemic inflammatory markers are associated with late-life brain volume: The ARIC study

✓ Peer-reviewed alzhub usefulness score 68 out of 100. Neurology 2017-11-01

Our prospective findings provide evidence for what may be an early contributory role of systemic inflammation in neurodegeneration and cognitive aging. 3 key findings →

Design: cohort study Participants: 1,633 Evidence: moderate

In this study, lower AD signature region volumes, brain microhemorrhages, higher WMH volumes, and infarcts were risk factors associated with dementia in older community-based residents. 4 key findings →

Design: cohort study Participants: 1,553 Evidence: moderate

Etiology of White Matter Hyperintensities in Autosomal Dominant and Sporadic Alzheimer Disease

✓ Peer-reviewed alzhub usefulness score 67 out of 100. JAMA neurology 2023-12-01

Data from 3960 MRI sessions among 1141 participants were included: 252 pathogenic variant carriers from DIAN (mean [SD] age, 38.4 [11.2] years; 137 [54%] female), 571 older adults from ADNI (mean [SD] age, 72.8 [7.3] years; 274 [48%] female), and 318 older adults from HABS (mean [SD] age, 72.4 [7.6] years; 194 [61%] female). 3 key findings →

Design: cohort study Participants: 1,141 Evidence: moderate

More-severe diabetes (defined by higher HbA 1c and longer disease duration) but not prediabetes or less-severe diabetes was associated with smaller brain volumes and an increased burden of brain vascular pathology. 3 key findings →

Design: cross-sectional Participants: 1,713 Evidence: low

Our main findings were: (i) FDG-PET uptake in the bilateral anterior cingulate cortex and anterior temporal pole was associated with baseline global cognition in cognitively stable 80+ (the resilience signature); (ii) established Alzheimer's disease imaging biomarkers did not predict baseline global cognition in this subset of participants; (iii) in the full MCSA 80+ and ADNI cohorts, amyloid burden and FDG-PET in the resilience signature were the stronger predictors of baseline global cognition; (iv) sex and systemic vascular health predicted FDG-PET in the resilience signature, suggesting vascular health maintenance as a potential pathway to preserve the metabolism of these areas; and (v) the resilience signature provided significant information about global longitudinal cognitive change even when considering amyloid status in both the MCSA and ADNI cohorts. 1 key finding →

Design: longitudinal study Participants: 192 Evidence: moderate

Dementia with Lewy bodies and Alzheimer disease: neurodegenerative patterns characterized by DTI

✓ Peer-reviewed alzhub usefulness score 63 out of 100. Neurology 2010-06-01

Increased amygdalar diffusivity in the absence of tissue loss in dementia with Lewy bodies (DLB) may be related to microvacuolation, a common pathology associated with Lewy body disease in the amygdala. 3 key findings →

Design: case-control study Participants: 30 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

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

Vascular burden and Alzheimer disease pathologic progression

✓ Peer-reviewed alzhub usefulness score 60 out of 100. Neurology 2012-09-12

Increased WMHs are associated with aging, decreased glucose metabolism, and decline in executive function but do not affect AD-specific pathologic progression, suggesting that the vascular contribution to dementia is probably additive although not necessarily independent of the amyloid pathway. 5 key findings →

Design: longitudinal study Evidence: moderate

Interestingly, we found no consistent differences in learning and memory performance between high versus low PiB cognitively normal or amnestic MCI subjects. 5 key findings →

Evidence: low

Comparison of different MRI brain atrophy rate measures with clinical disease progression in AD

✓ Peer-reviewed alzhub usefulness score 59 out of 100. Neurology 2004-02-01

These data support the use of rates of change from serial MRI studies in addition to standard clinical/psychometric measures as surrogate markers of disease progression in AD. 1 key finding →

Participants: 55 Evidence: low

Symptomatic mutation carriers also demonstrated elevated tau PET binding in the basal ganglia, consistent with prior work with amyloid-β. 2 key findings →

Design: cross-sectional Evidence: low

Rates of brain atrophy and/or ventricular enlargement were correlated with declining performance on cognitive scales. 2 key findings →

Design: longitudinal study 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 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