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Find studies

Showing 1–25 of 207 studies in Brain scans and imaging (page 1 of 9) · 27,380 in the whole library · How the 0–100 score works

Showing 207 studies tagged positron — clear

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

Longitudinal 18F-MK-6240 tau tangles accumulation follows Braak stages

✓ Peer-reviewed alzhub usefulness score 71 out of 100. Brain : a journal of neurology 2021-12-01

We found that the cognitively unimpaired amyloid-β-negative individuals had significant longitudinal tau accumulation confined to the PET Braak-like stage I (3.9%) and II (2.8%) areas. 4 key findings →

Design: longitudinal study Participants: 125 Evidence: moderate

The best-performing MRI-free approaches had high continuous and dichotomous agreement with MRI-dependent SUVRs for Aβ PET and temporal flortaucipir (R2 ≥0.95; ± agreement ≥92%) and for Alzheimer's disease-related effect sizes; agreement was slightly lower for entorhinal flortaucipir and longitudinal slopes. 2 key findings →

Design: longitudinal study Participants: 1,290 Evidence: moderate

There were 571 participants in the normal cognition group, 625 participants in the subjective cognitive decline group, 155 participants in the objectively defined subtle cognitive decline group, 501 participants in the mild cognitive impairment group, 471 participants in Alzheimer's disease group, and 128 participants with cognitive impairment from other known causes. 5 key findings →

Design: longitudinal study Participants: 4,386 Evidence: moderate

Participants with CIND displayed lower perfusion in the PCC+PCu relative to participants who were CN, but there was no statistically significant difference between the groups in amyloid burden in this region. 5 key findings →

Design: case-control study Participants: 113 Evidence: moderate

CL was associated with syndromic (F = 4.42, p = 0.014) and etiological diagnosis (F = -12.66, p < 0.001), with Alzheimer's disease (AD) patients showing the highest amyloid burden (62.9 ± 27.5), followed by dementia with Lewy bodies (DLB) (25.3 ± 35.5) and cardiovascular disease (CVD) (16.7 ± 24.5), and finally frontotemporal lobe degeneration (FTLD) (5.0 ± 17.22, t = -12.66, p < 0.001). 4 key findings →

Design: longitudinal study Participants: 157 Evidence: moderate

Amyloid chronicity provides unique information about cognitive decline and neurofibrillary tangle development and may be useful to investigate preclinical Alzheimer's disease. 2 key findings →

Design: longitudinal study Participants: 257 Evidence: moderate

Primary include several amyloid PET measurements (Centiloid, SUVr, BPND , R1 ), and secondary are their changes from baseline, relationship to other amyloid markers (cerebrospinal fluid and visual assessment), and predictive value of AD-related decline. 2 key findings →

Design: cohort study Participants: 2,000 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

As cerebral regions correlating with symptomatology differ depending on the clinical phenotype, a precise knowledge of clinical signs and symptoms is necessary when interpreting [18F]PI-2620 PET results. 1 key finding →

Design: longitudinal study Participants: 72 Evidence: moderate

The annual increase of flortaucipir SUVr was greater in the middle and superior occipital, fusiform, and inferior parietal cortices in DLB (mean: 0.017, 0.019, 0.019, and 0.015, respectively) compared with the CU (mean: -0.006, -0.009, -0.003, and - 0.005, respectively; P < 0.05). 5 key findings →

Design: longitudinal study Participants: 22 Evidence: moderate

Cortical tau accumulation is a key pathological event that partly defines Alzheimer's disease (AD) onset and is associated with cognitive decline and future disease progression. 5 key findings →

Design: cohort study Participants: 59 Evidence: moderate

Increased retention of tau PET ligand [18F]-AV1451 in Alzheimer's Disease Psychosis

✓ Peer-reviewed alzhub usefulness score 64 out of 100. Translational psychiatry 2022-02-26

Psychosis in Alzheimer's disease (AD) represents a distinct disease subtype with a more rapid progression of illness evidenced by an increased velocity of cognitive decline and a hastened mortality. 2 key findings →

Design: longitudinal study Participants: 17 Evidence: moderate

Tau positron emission tomography (PET) imaging allows in vivo detection of tau proteinopathy in Alzheimer's disease, which is associated with neurodegeneration and cognitive decline. 3 key findings →

Participants: 12,048 Evidence: low

For amyloid positron emission tomography positive (Aβ+) subjects, flortaucipir neocortical standard uptake value ratio was significantly higher with more advanced clinical stage (Alzheimer's disease > mild cognitive impairment > older cognitively normal) and was significantly elevated for Aβ+ mild cognitive impairment and Alzheimer's disease subjects relative to the respective Aβ- subjects. 5 key findings →

Design: cross-sectional Participants: 217 Evidence: low

SPARE-Tau: A flortaucipir machine-learning derived early predictor of cognitive decline

✓ Peer-reviewed alzhub usefulness score 61 out of 100. PloS one 2022-11-03

Compared to CSF p-tau, meta-temporal, and averaged Braak tau PET ROIs, SPARE-Tau showed the strongest association with baseline ADAS-cog13 scores and diagnosis. 5 key findings →

Design: cross-sectional Participants: 587 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

In the cross-sectional study, CLs in both the Aβ- and the Aβ+ groups were impacted by the FWHM of the reconstruction method. 5 key findings →

Design: cross-sectional Participants: 89 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