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Find studies

Showing 2,901–2,925 of 2,940 studies · tagged Brain Scans (page 117 of 118) · 28,180 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.

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.

: Treated patients were 74±7 years old; 57% were female, 59% were apolipoprotein E ε4 carriers, and 78% had mild cognitive impairment (22% mild dementia). 5 key findings →

Participants: 15 Evidence: low

Regional Cerebrospinal Fluid Motility as a Key Determinant of Soluble Amyloid-β Levels and Kinetics

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-08-03

Alzheimer’s disease and cerebral amyloid angiopathy are characterized by the accumulation of amyloid-β (Aβ) species, yet the human fluid-physiological mechanisms that regulate soluble Aβ transport and clearance remain poorly understood. 3 key findings →

Participants: 502 Evidence: moderate

As the world's population ages, Alzheimer's disease (AD), a progressive neurodegenerative disorder, is becoming more common. 1 key finding →

Participants: 59 Evidence: low

Residualized WMH T1w/T2w-FLAIR ratio captures lesion-specific microstructural variation missed by volumetric measures, consistent with vascular-gliotic injury in VD and coexisting amyloid-linked demyelination in AD. 4 key findings →

Design: cross-sectional Participants: 71 Evidence: moderate

Investigating the Amyloid-Tau-Neurodegeneration Framework in Alzheimer’s Disease Using Semi-Supervised Multimodal Imaging Data Fusion

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-12-15

Semi-supervised multimodal fusion improves prediction and reveals interpretable imaging patterns that predict APOE4 and clinical diagnoses better than traditional approaches. 2 key findings →

Evidence: low

Functional neuroimaging as a tool to understand social determinants of health in cognitive aging and ADRD: a scoping review

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. PsyArXiv 2026-10-20

The social, structural, and physical conditions in which individuals live, work, and age, collectively termed social determinants of health (SDOH), are associated with risk of Alzheimer's disease and related dementias (ADRD). 2 key findings →

Design: cross-sectional Evidence: low

Neuropsychiatric symptoms (NPS) are highly prevalent in Mild Cognitive Impairment (MCI), conceptualized as an intermediate clinical state between normal aging and dementia. 4 key findings →

Design: longitudinal study Evidence: moderate

Alzheimer’s disease (AD) pathology is increasingly recognized to manifest in the retina, offering a non-invasive window for early biomarker discovery. 2 key findings →

Design: longitudinal study Participants: 40 Evidence: moderate

MRI measures of cortical microstructural damage associate with tau accumulation in presymptomatic Alzheimer’s disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2025-12-16

NODDI-derived ODI is associated with tau PET signal, even in preclinical disease and may discriminate individuals with-and without tau beyond the MTL. 3 key findings →

Evidence: low

Real-World Characterization of Amyloid-Related Imaging Abnormalities (ARIA) in Lecanemab Treatment at an Academic Health System

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-01-25

The overall incidence of any ARIA was 25.2%, with ARIA-H occurring in 22.4% of patients and ARIA-E in 12.2%. 3 key findings →

Design: cohort study Participants: 468 Evidence: moderate

Temporal imaging variables may provide independent prognostic information beyond baseline risk, supporting a dynamic model of haemorrhagic risk in Alzheimer’s disease. 2 key findings →

Participants: 1,069 Evidence: low

ScFv-h3D6 Prevents Bapineuzumab-Induced Hemorrhagic Events in the APP23 Mouse Model of Alzheimer’s Disease

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Preprints.org 2025-11-05

The occurrence of amyloid-related imaging abnormalities (ARIA), found in clinical trials for Aβ-immunotherapy, has been related to the antibody’s effector function on glial activation by the Fc portion of the antibody. 2 key findings →

Evidence: low

DESI is a robust, fully automated MRI biomarker that sensitively detects CSF redistribution characteristic of DESH in iNPH. 1 key finding →

Design: longitudinal study Participants: 1,032 Evidence: moderate

Subacute and Chronic Cognitive and Cerebrovascular Functional Consequences of Mild Traumatic Brain Injury in Rats

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-07-27

Traumatic brain injury (TBI) is the main cause of death and disability in the United States in people younger than 35 years old and is a common cause of wartime injuries. 1 key finding →

Evidence: low

In this bvFTD cohort, structural volumes of key frontotemporal and perisylvian regions did not predict behavioral or language impairments after correction for multiple comparisons. 3 key findings →

Design: longitudinal study Participants: 87 Evidence: moderate

High-content imaging of live microglia-containing Alzheimer’s disease brain organoids

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. bioRxiv 2026-10-27

This method establishes a platform for high-throughput longitudinal drug screening in immunocompetent human COs that will enable the identification of new therapeutic candidates to modulate Aβ aggregation, glial reactivity, and neurodegeneration. 5 key findings →

Design: longitudinal study Evidence: moderate

Contribution of cerebrovascular lesions to neurodegeneration and cognitive decline

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. medRxiv 2026-10-06

Vascular risk factors were associated with CSVD burden and progression, and WMH and PVS progression were further associated with cortical atrophy and cognitive decline, underscoring the interconnected contributions of vascular risk, CSVD, and neurodegeneration to cognitive aging and dementia risk. 5 key findings →

Design: cross-sectional Participants: 289 Evidence: moderate

Multimodal integration of cognitive, neuroimaging, and polygenic data in the MHS-RWD tool yields strong discrimination for both early diagnosis of dementia and AD differential diagnosis. 2 key findings →

Participants: 1,100 Evidence: low

Pain is independently associated with agitation and neuropsychiatric symptoms in Alzheimer’s disease: a cross-sectional MRI study

⚠ Preprint — not yet peer-reviewed alzhub usefulness score 16 out of 100. Research Square 2026-09-15

Significant positive correlations were observed among pain, cognitive impairment, agitation, and neuropsychiatric symptoms (all p < 0.001). 4 key findings →

Participants: 107 Evidence: low

From across this tag

9 of the 2,925 studies in this tag, picked by a fixed rule (a hash of each study's address), not by score or date; each page of this list shows a different 9. The same 9 appear here every time.

↑ Change the filters

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