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Find studies

Showing 501–525 of 566 studies in Lewy body dementia (page 21 of 23) · 27,380 in the whole library · How the 0–100 score works

Browse by subject, author or institution

Each number is how many studies that link shows, with your other filters kept.

What “Lewy body dementia” covers

Lewy body dementia — Dementia with Lewy bodies and related conditions: how they differ from Alzheimer's in symptoms, diagnosis and care.

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.

The thematic analysis identified 12 themes: manifestations, sexual practices, impact, control, emotional formulations, beliefs in causes of hypersexuality and attributions, relationship with the partner, dealing with hypersexuality, coping with hypersexuality, self-image, stigma and professional help-seeking. 5 key findings →

Evidence: low

The drive for positive social interactions, or "social rewards", is an important motivator of human behaviour, conferring several adaptive benefits. 5 key findings →

Evidence: low

Multiplex connectomics reveal altered networks in frontotemporal dementia: A multisite study

✓ Peer-reviewed alzhub usefulness score 40 out of 100. Network Neuroscience 2025-01-01

A network neuroscience perspective can significantly advance the understanding of neurodegenerative disorders, particularly frontotemporal dementia (FTD). 5 key findings →

Participants: 28 Evidence: moderate

We dissociated four key cognitive components underlying remote thinking: spontaneous associative thinking, inhibition of unoriginal responses, intentional remote associative thinking, and verbal initiation; and replicated them in three independent datasets. 5 key findings →

Evidence: low

Emerging evidence implicating glymphatic dysfunction contributes to the pathogenesis of frontotemporal dementia (FTD). 3 key findings →

Participants: 37 Evidence: low

Frontotemporal dementia (FTD) encompasses a broad, clinically and neuropathologically diverse group of neurodegenerative disorders associated with changes in personality, behaviour, and/or language due to the progressive degeneration of the frontal and temporal lobes of the brain. 3 key findings →

Evidence: low

Lewy bodies and neurofibrillary tangles, composed of α-synuclein (α-syn) and tau, respectively, often are found together in the same brain and correlate with worsening cognition. 3 key findings →

Evidence: low

Onset-predictive biomarker tests (OPBTs) for genetic frontotemporal dementia (FTD) may predict symptom onset in coming years. 4 key findings →

Evidence: low

Tau mutant cortical organoids showed altered mitochondrial function and gene expression related to neuronal development, with synaptic markers and neuronal activity reduction. 5 key findings →

Evidence: low

In addition to the core clinical features of fluctuating cognition, visual hallucinations, and parkinsonism, individuals with dementia with Lewy bodies (DLB) frequently experience chronic and debilitating major depression. 2 key findings →

Evidence: low

= 62.87, SD = 9.46, 36.52% female). Both networks were densely connected, reflecting comorbidity between neuropsychiatric symptoms and cognitive scores. 5 key findings →

Evidence: low

Lewy body dementia (LBD) is a neurodegenerative disorder characterized by a combination of progressive dementia and spontaneous parkinsonian symptoms. 5 key findings →

Evidence: low

These models demonstrated high diagnostic efficacy in distinguishing diseased samples from healthy donors as well as distinguishing AD and DLB cases. 3 key findings →

Evidence: low

Frontotemporal dementia (FTD) refers to a group of neurodegenerative disorders characterized clinically by behavioral disturbances and pathologically by frontal and anterior temporal lobe neurodegeneration, resulting in brain atrophy. 5 key findings →

Evidence: high

The incidence of dementia, and specifically, Alzheimer's disease, is higher in women than men, even in middle age, making it possible to rule out lifespan differences between men and women as a contributing factor. 5 key findings →

Evidence: low

Graphene quantum dots prevent α-synucleinopathy in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Nature nanotechnology 2018-07-09

Though emerging evidence indicates that the pathogenesis of Parkinson's disease is strongly correlated to the accumulation 1,2 and transmission 3,4 of α-synuclein (α-syn) aggregates in the midbrain, no anti-aggregation agents have been successful at treating the disease in the clinic. 1 key finding →

Evidence: low

< .01). All patient groups were also impaired on AVLT encoding, TMT-B and TMT B/A. Social and non-social neurocognitive functions differed between groups, with specific impairments in processing speed in VaD, emotion recognition in bv-FTD and memory retrieval in AD, and memory encoding and cognitive control impaired in all three groups. 4 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 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