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Find studies

Showing 701–725 of 894 studies in Brain scans and imaging · tagged Brain Scans (page 29 of 36) · 28,580 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.

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.

Aggregation of amyloid-β (Aβ) as toxic oligomers and amyloid plaques within the brain appears to be the pathogenic event that initiates Alzheimer's disease (AD) lesions. 2 key findings →

Evidence: low

The findings suggest that CA1 measurement is more sensitive than global hippocampal volumetry to detect structural changes at the pre-dementia stage, although the predominance of CA1 atrophy does not appear to be specific to AD pathophysiological processes. 5 key findings →

Evidence: low

The in vivo imaging probe [11C]-PIB (Pittsburgh Compound B, N-methyl[11C]2-(4'-methylaminophenyl-6-hydroxybenzathiazole) is under evaluation as a key imaging tool in Alzheimer's disease (AD) and to date has been assumed to bind with high affinity and specificity to the amyloid structures associated with classical plaques (CPs), one of the pathological hallmarks of the disease. 3 key findings →

Evidence: low

Network analysis of intrinsic functional brain connectivity in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. PLoS computational biology 2008-06-27

Functional brain networks detected in task-free ("resting-state") functional magnetic resonance imaging (fMRI) have a small-world architecture that reflects a robust functional organization of the brain. 3 key findings →

Evidence: low

TDP-43 is a key player in the clinical features associated with Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Acta neuropathologica 2014-03-23

The aim of this study was to determine whether the TAR DNA-binding protein of 43 kDa (TDP-43) has any independent effect on the clinical and neuroimaging features typically ascribed to Alzheimer's disease (AD) pathology, and whether TDP-43 pathology could help shed light on the phenomenon of resilient cognition in AD. 2 key findings →

Evidence: low

Hierarchical feature representation and multimodal fusion with deep learning for AD/MCI diagnosis

✓ Peer-reviewed alzhub usefulness score 40 out of 100. NeuroImage 2014-07-18

For the last decade, it has been shown that neuroimaging can be a potential tool for the diagnosis of Alzheimer's Disease (AD) and its prodromal stage, Mild Cognitive Impairment (MCI), and also fusion of different modalities can further provide the complementary information to enhance diagnostic accuracy. 3 key findings →

Evidence: low

Medial temporal lobe function and structure in mild cognitive impairment

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Annals of neurology 2004-07-01

Functional magnetic resonance imaging (fMRI) was used to study memory-associated activation of medial temporal lobe (MTL) regions in 32 nondemented elderly individuals with mild cognitive impairment (MCI). 1 key finding →

Evidence: low

Functions of the Alzheimer's Disease Neuroimaging Initiative (ADNI) magnetic resonance imaging (MRI) core fall into three categories: (1) those of the central MRI core laboratory at Mayo Clinic, Rochester, Minnesota, needed to generate high quality MRI data in all subjects at each time point; (2) those of the funded ADNI MRI core imaging analysis groups responsible for analyzing the MRI data; and (3) the joint function of the entire MRI core in designing and problem solving MR image acquisition, pre-processing, and analyses methods. 5 key findings →

Evidence: low

Recent imaging evidence in Alzheimer's disease suggests that neural involvement in early-stage disease is more complex than is encapsulated in the commonly held position of predominant mesial temporal lobe degeneration-there is also early posterior cingulate cortex and diencephalic damage. 5 key findings →

Evidence: low

The topography of grey matter involvement in early and late onset Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Brain : a journal of neurology 2007-02-09

Clinical observations have suggested that the neuropsychological profile of early and late onset forms of Alzheimer's disease (EOAD and LOAD) differ in that neocortical functions are more affected in the former and learning in the latter, suggesting that they might be different diseases. 2 key findings →

Evidence: low

Direct voxel-based comparison between grey matter hypometabolism and atrophy in Alzheimer's disease

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Brain 2007-12-03

Although the patterns of structural and metabolic brain alterations in Alzheimer's disease are being refined and discrepancies between them are being underlined, the exact relationships between atrophy and hypometabolism are still unclear. 3 key findings →

Evidence: low

PET amyloid imaging is increasingly used in research trials related to Alzheimer disease and has potential as a quantitative biomarker. 1 key finding →

Evidence: low

Pallidal lesions in patients with liver cirrhosis: clinical and MRI evaluation

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Metabolic brain disease 1995-09-01

Fifty patients with liver cirrhosis underwent neurological, psychometric, electroencephalographic and biochemical examination as well as cranial magnetic resonance imaging (MRI) to study the incidence of pallidal lesions in cirrhotics and their correlation to liver function, as well as to neurological and mental state. 5 key findings →

Evidence: low

Region specific correlations between corpus callosum size and EEG coherence suggest that the decline in interhemispheric connectivity in Alzheimer's disease results from a specific loss of cortical association neurones projecting through the corpus callosum. 3 key findings →

Evidence: low

Juxtacortical free water fraction, determined at diffusion MRI, was higher in participants with Alzheimer disease compared with cognitively normal controls and associated with amyloid-β, tau, and neurodegeneration biomarkers, revealing two distinct spatiotemporal progression patterns with different impacts on neuroanatomic signatures and cognitive performance. 1 key finding →

Evidence: low

Alzheimer\\\'s disease (AD), the leading cause of dementia worldwide, affects more than 55 million individuals and gen-erates annual healthcare costs exceeding two trillion USD [14]. 5 key findings →

Design: longitudinal study Evidence: moderate

EARLY STAGES OF ALZHEIMERS DETECTION

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Zenodo (CERN European Organization for Nuclear Research) 2025-11-20

The Early Stages of Alzheimer’s Detection project focuses on identifying signs of Alzheimer’s disease at the earliest possible stage using advanced machine learning and medical imaging techniques. 3 key findings →

Evidence: low

EARLY STAGES OF ALZHEIMERS DETECTION

✓ Peer-reviewed alzhub usefulness score 39 out of 100. Zenodo (CERN European Organization for Nuclear Research) 2025-11-20

The Early Stages of Alzheimer’s Detection project focuses on identifying signs of Alzheimer’s disease at the earliest possible stage using advanced machine learning and medical imaging techniques. 3 key findings →

Evidence: low

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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 28,580 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 28,580 records, built mostly from automated pulls of Europe PMC (62.2% of the library) and OpenAlex (17.8%), 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 (3.6% 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