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Find studies

Showing 101–125 of 237 studies in Brain scans and imaging · tagged Other Dementias (page 5 of 10) · 32,180 in the whole library · How the 0–100 score works

Download bibliography of these 237 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.

Pick-type histology was seen in 14 cases (21%) and tau histological changes associated with frontotemporal dementia (FTD) linked to chromosome 17 (FTDP-17) were present in 11 cases (16%). 5 key findings →

Participants: 70 Evidence: low

Testing an aetiological model of visual hallucinations in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Brain : a journal of neurology 2011-09-15

When corrected for multiple comparisons, patients with visual hallucinations had significantly greater disease duration, treatment duration, motor severity and complications, sleep disturbances, in particular excessive daytime somnolence and rapid eye movement sleep behavioural disorder, disorders of mood, autonomic dysfunction and global, frontal and visuoperceptive cognitive dysfunction. 3 key findings →

Participants: 94 Evidence: low

We reviewed the polysomnograms (PSGs) of 292 consecutive patients with sleep disorders (Parkinson's disease (PD), n=19, other sleep disorders, n=273) to investigate the sensitivity and specificity of the clinical diagnosis of rapid eye movement behavior disorder (RBD) compared with polysomnographic diagnosis. 3 key findings →

Participants: 19 Evidence: low

PRD was associated with selective disruption of corticostriatal resting functional MR imaging correlations, which suggests that resting functional MR imaging analyzed in subject-native space may be a useful biomarker in this disease. 5 key findings →

Participants: 19 Evidence: moderate

We found no significant changes in substantia nigra or cortex flortaucipir uptake in Parkinson's disease patients over two years and no association with changes in cognitive symptoms. 3 key findings →

Design: cross-sectional Evidence: low

Intrinsic connectivity networks in posterior cortical atrophy: A role for the pulvinar?

✓ Peer-reviewed alzhub usefulness score 46 out of 100. NeuroImage. Clinical 2018-12-03

Patients with PCA showed disproportionate deficits in the visuospatial domain; they also showed preserved social sensitivity and endorsed more depressive symptoms than HCs. 5 key findings →

Participants: 26 Evidence: low

A 7-min window, corresponding to minutes 1-8 (frames 5-15), produced the highest voxelwise correlation between (18)F-FDG and pPIB (R = 0.78 ± 0.05). 4 key findings →

Evidence: moderate

Resting state functional magnetic resonance imaging (fMRI) was used to measure whole brain functional connectivity within specific networks hypothesised to be more affected in dementia with Lewy bodies (DLB) (a disease characterised by prominent attentional deficits, spontaneous motor features of parkinsonism and depression) than in Alzheimer׳s disease (AD) and controls. 4 key findings →

Participants: 68 Evidence: low

Tau PET imaging in neurodegenerative tauopathies-still a challenge

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Molecular psychiatry 2019-01-11

The accumulation of pathological misfolded tau is a feature common to a collective of neurodegenerative disorders known as tauopathies, of which Alzheimer's disease (AD) is the most common. 5 key findings →

Evidence: low

AV-1451 is more sensitive and specific to Alzheimer's disease type tau and shows lower off-target binding, while THK5351 may mirror non-specific neurodegeneration. 1 key finding →

Design: cross-sectional Evidence: low

Early microglial activation and peripheral inflammation in dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 45 out of 100. Brain : a journal of neurology 2018-12-01

Microglial activation was elevated in dementia with Lewy bodies subjects with mild disease when compared to those with moderate/severe impairment, where disease severity was indexed by cognitive performance on the revised Addenbrooke's Cognitive Examination. 4 key findings →

Evidence: low

We describe a family with nearly 300 members over 8 generations with 32 affected individuals who have an autosomal dominant neurodegenerative disease characterized by progressive parkinsonism with dystonia unrelated to medications, dementia, ocular motility abnormalities, pyramidal tract dysfunction, frontal lobe release signs, perseverative vocalizations, and urinary incontinence. 1 key finding →

Evidence: low

Behavioral variant frontotemporal dementia (bvFTD) disrupts our most human social and emotional functions. 2 key findings →

Evidence: low

We compare patterns of gray matter loss on MRI in subjects presenting as corticobasal syndrome (CBS) with Alzheimer disease pathology (CBS-AD) to those presenting as CBS with corticobasal degeneration pathology (CBS-CBD). 4 key findings →

Evidence: low

Eating behavior in frontotemporal dementia: Peripheral hormones vs hypothalamic pathology

✓ Peer-reviewed alzhub usefulness score 43 out of 100. Neurology 2015-09-16

In bvFTD, they are in part related to hypothalamic degeneration, with potential disintegration of the network connections between the hypothalamus and orbitofrontal cortex/reward pathways. 1 key finding →

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
  • Randomized / 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
  • Multicenter 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 32,180 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 32,180 records, built mostly from automated pulls of Europe PMC (66.5% of the library) and OpenAlex (15.8%), 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.

1,045 records (3.2% of the library) are not peer-reviewed — 966 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    Where this research is being discussed: events

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