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Find studies

Showing 326–350 of 610 studies · free to read (page 14 of 25) · 30,580 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)

Showing 610 studies tagged frontotemporal — clear

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.

Behavioural-variant frontotemporal dementia: diagnosis, clinical staging, and management

✓ Peer-reviewed alzhub usefulness score 50 out of 100. The Lancet. Neurology 2010-12-10

Patients with behavioural-variant frontotemporal dementia (bvFTD) present with insidious changes in personality and interpersonal conduct that indicate progressive disintegration of the neural circuits involved in social cognition, emotion regulation, motivation, and decision making. 5 key findings →

Evidence: low

MRI and pathology of REM sleep behavior disorder in dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Neurology 2013-10-09

Patients with autopsy-confirmed low-, intermediate-, and high-likelihood DLB, according to the probability statement recommended by the third report of the DLB Consortium, and antemortem MRI, were identified (n = 75). 3 key findings →

Participants: 75 Evidence: low

Distinctive Oculomotor Behaviors in Alzheimer's Disease and Frontotemporal Dementia

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Frontiers in aging neuroscience 2021-02-04

Oculomotor behavior can provide insight into the integrity of widespread cortical networks, which may contribute to the differential diagnosis between Alzheimer's disease and frontotemporal dementia. 2 key findings →

Participants: 93 Evidence: low

Although diagnosed by characteristic motor features, Parkinson's disease may be preceded, and is frequently accompanied by, a wide range of cognitive and neuropsychiatric features. 1 key finding →

Evidence: low

Lewy bodies (LBs) are alpha-synuclein-immunoreactive neuronal inclusions with a predilection for specific cortical and subcortical regions, including the amygdala. 2 key findings →

Evidence: low

TDP-43 pathology in Alzheimer's disease, dementia with Lewy bodies and ageing

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Brain pathology (Zurich, Switzerland) 2016-08-24

Intracellular inclusions consisting of TAR DNA binding protein-43 (TDP-43 pathology) are present in up to 57% of Alzheimer's disease (AD) cases and follow a distinct topographical pattern of progression described in the TDP-43 in AD staging scheme. 4 key findings →

Evidence: low

A patient journey analysis: Identification and treatment of dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Alzheimer s & Dementia 2020-12-01

Percentages of patients with imaging tests, DLB symptoms, diagnoses and treatments for DLB increased as patients’ first DLB diagnosis neared and occurred at lower percentages 7‐12 months after initial diagnosis. 1 key finding →

Design: systematic review Participants: 974 Evidence: high

This narrative review examines the utility of gait digital biomarkers in Parkinson's disease (PD) research and clinical trials across four contexts: disease susceptibility/risk, disease progression, response to exercise, and fall prediction. 1 key finding →

Design: narrative review Evidence: low

The identification of biomarkers predicting the burden of brain alpha-synuclein (α-syn) pathology in vivo represents a research priority in Lewy body disease (LBD). 5 key findings →

Evidence: low

Of 11 subjects with average AUCs above 500,000 units, 7 (64%) developed a central LBD compared to 1 of 20 (5%), with AUCs below the cutoff value (P = 0.0011 by log-rank test). 3 key findings →

Design: longitudinal study Evidence: moderate

Key motor and non-motor features in early dementia with Lewy bodies

✓ Peer-reviewed alzhub usefulness score 50 out of 100. Frontiers in Neurology 2025-03-13

Early-stage DLB closely resembles PD in motor symptoms but has more neuropsychiatric non-motor symptoms compared to PD and overall non-motor symptoms than AD. 3 key findings →

Design: cross-sectional Participants: 107 Evidence: low

A hexanucleotide repeat expansion in the C9orf72 gene is the most common genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) with synaptic dysfunction identified as an early pathological hallmark. 3 key findings →

Design: meta-analysis Evidence: high

A critical evaluation of the Braak staging scheme for Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Annals of neurology 2008-11-01

Braak and colleagues have proposed that, within the central nervous system, Parkinson's disease (PD) begins as a synucleinopathy in nondopaminergic structures of the lower brainstem or in the olfactory bulb. 1 key finding →

Evidence: low

Brain connectivity in neurodegenerative diseases--from phenotype to proteinopathy

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nature reviews. Neurology 2014-10-07

Functional and structural connectivity measures, as assessed by means of functional and diffusion MRI, are emerging as potential intermediate biomarkers for Alzheimer disease (AD) and other disorders. 2 key findings →

Evidence: low

We report the clinical, neuroimaging, and neuropathologic characteristics of 2 patients who developed early onset dementia after a moderate-severe traumatic brain injury (TBI). 3 key findings →

Evidence: low

Frontotemporal lobar degeneration proteinopathies with tau inclusions (FTLD-Tau) or TDP-43 inclusions (FTLD-TDP) are associated with clinically similar phenotypes. 3 key findings →

Participants: 92 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.

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 30,580 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 30,580 records, built mostly from automated pulls of Europe PMC (64.7% of the library) and OpenAlex (16.6%), 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.

1,037 records (3.4% of the library) are not peer-reviewed — 964 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