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Find studies

Showing 351–375 of 566 studies in Lewy body dementia (page 15 of 23) · 29,780 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 “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.

Evidence for divergent cortical organisation in Parkinson’s disease and Lewy Body Dementia

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Nature Communications 2025-11-25

Dementia is a defining feature of Lewy body disease: its timing and onset distinguish different clinical diagnoses, and its effect on quality of life is profound. 1 key finding →

Participants: 108 Evidence: low

Males were more likely than females to present with two or more core DLB clinical features 2 years prior to obtaining a diagnosis of dementia. 5 key findings →

Design: longitudinal study Evidence: moderate

Preclinical Catecholaminergic Biomarkers of Central Lewy Body Diseases

✓ Peer-reviewed alzhub usefulness score 49 out of 100. Journal of Clinical Neurology 2026-01-01

In the central Lewy body diseases (LBDs) Parkinson's disease and dementia with Lewy bodies (DLB), by the time parkinsonism or cognitive dysfunction manifests, substantial central neurodegeneration has already occurred. 5 key findings →

Design: longitudinal study Evidence: moderate

Immunotherapies for various neurodegenerative diseases have recently emerged as a promising approach for clearing pathological protein conformers in these disorders. 5 key findings →

Evidence: low

There's Something Wrong with my MAM; the ER-Mitochondria Axis and Neurodegenerative Diseases

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Trends in neurosciences 2016-02-15

Alzheimer's disease (AD), Parkinson's disease (PD), and amyotrophic lateral sclerosis with associated frontotemporal dementia (ALS/FTD) are major neurodegenerative diseases for which there are no cures. 1 key finding →

Evidence: low

Pathologic alterations in the microtubule-associated protein tau have been implicated in a number of neurodegenerative disorders, including Alzheimer's disease (AD), progressive supranuclear palsy (PSP), and frontotemporal dementia (FTD). 1 key finding →

Evidence: low

Tandem repeats mediating genetic plasticity in health and disease

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Nature reviews. Genetics 2018-02-05

Accumulating evidence suggests that many classes of DNA repeats exhibit attributes that distinguish them from other genetic variants, including the fact that they are more liable to mutation; this enables them to mediate genetic plasticity. 2 key findings →

Evidence: low

Microglia, the immunocompetent cells of the central nervous system (CNS), act as neuropathology sensors and are neuroprotective under physiological conditions. 5 key findings →

Evidence: low

Although aberrant microRNA (miRNA) expression is linked to human diseases including cancer, the mechanisms that regulate the expression of each individual miRNA remain largely unknown. 1 key finding →

Evidence: low

Hyperphosphorylation of the microtubule-associated protein tau is specifically found in those brain cells affected in several tauopathies. 2 key findings →

Evidence: low

Frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. The Lancet. Neurology 2005-11-01

Frontotemporal dementia (FTD) is a focal clinical syndrome characterised by profound changes in personality and social conduct and associated with circumscribed degeneration of the prefrontal and anterior temporal cortex. 1 key finding →

Evidence: low

Cytoplasmic deposition of alpha-synuclein aggregates is a common pathological feature of many neurodegenerative diseases. 2 key findings →

Evidence: low

The Lewy body in Parkinson's disease and related neurodegenerative disorders

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Molecular neurobiology 2012-05-24

The histopathological hallmark of Parkinson's disease (PD) is the presence of fibrillar aggregates referred to as Lewy bodies (LBs), in which α-synuclein is a major constituent. 1 key finding →

Evidence: low

Previous studies demonstrate that intrastriatal injections of fibrillar alpha-synuclein (α-syn) into mice induce Parkinson's disease (PD)-like Lewy body (LB) pathology formed by aggregated α-syn in anatomically interconnected regions and significant nigrostriatal degeneration. 5 key findings →

Evidence: low

TDP-43 is a multifunctional DNA/RNA-binding protein that has been identified as the major component of the cytoplasmic ubiquitin (+) inclusions (UBIs) in diseased cells of frontotemporal lobar dementia (FTLD-U) and amyotrophic lateral sclerosis (ALS). 3 key findings →

Evidence: low

Cholinergic degeneration and early cognitive signs in prodromal Lewy body dementia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer s & Dementia 2025-02-01

cBF volume declined at comparable rates in iRBD-to-PD and iRBD-to-DLB converters, but atrophy was more severe at DLB phenoconversion. cBF atrophy correlated with attention, executive, and memory deficits. 5 key findings →

Design: cross-sectional Evidence: moderate

Dementia with Lewy bodies (DLB) frequently coexists with Alzheimer's disease pathology, yet the pattern of cortical microstructural injury and its relationship with amyloid, tau, and cerebrovascular pathologies remains unclear. 3 key findings →

Participants: 57 Evidence: low

White matter hyperintensities precede other biomarkers in GRN frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer s & Dementia 2025-10-01

Symptomatic GRN carriers showed elevated WMHs, primarily in the frontal lobe, while no significant increase was observed in symptomatic C9orf72 or MAPT carriers. 5 key findings →

Participants: 763 Evidence: low

Of 43 individuals enrolled, 14 were women (33%); age (mean ± SD) was 73 ± 8.5 years. 5 key findings →

Design: clinical trial Participants: 43 Evidence: high

Quantitative susceptibility mapping reveals differences between subtypes of Lewy body dementia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Brain 2025-09-03

Dementia with Lewy bodies (DLB) and Parkinson's disease dementia (PDD) are subtypes of Lewy body dementia, and are considered two ends of a disease spectrum. 5 key findings →

Participants: 66 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 29,780 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 29,780 records, built mostly from automated pulls of Europe PMC (63.8% of the library) and OpenAlex (17.1%), 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.

1,037 records (3.5% 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