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Research

27,380 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 376–400 of 566 studies in Lewy body dementia (page 16 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.

Other subjects

Authors

Names as each record prints them; the same person can appear under two spellings.

Institutions

From OpenAlex; 12,859 studies have no institution on record and are not counted here.

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.

Sex differences for regional pathology in people with a high likelihood of Lewy body dementia phenotype based on underlying pathology

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring 2025-01-01

Sex differences for clinicopathological correlations in LBD also occur at the regional pathology level. 3 key findings →

Participants: 357 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Distinctive Progression Patterns of Brain Structural Damage Aid Classification of Frontotemporal Dementia Variants

✓ Peer-reviewed alzhub usefulness score 48 out of 100. European Journal of Neurology 2025-09-01

At baseline, sbvFTD showed right-predominant temporal pole involvement associated with significant right frontal atrophy. 5 key findings →

Design: longitudinal study Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Cerebrovascular co-pathology and cholinergic white matter pathways along the Lewy body continuum

✓ Peer-reviewed alzhub usefulness score 48 out of 100. Brain Communications 2025-01-01

Lewy body patients showed a significantly higher degree of WMSA in the external capsule cholinergic pathway despite no significant differences in global WMSA compared to controls. 4 key findings →

Participants: 82 Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

TDP-43-mediated alternative polyadenylation is associated with a reduction in VPS35 and VPS29 expression in frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 48 out of 100. PLoS Biology 2026-01-05

TAR DNA-binding protein 43 (TDP-43) dysfunction is a hallmark of several neurodegenerative diseases, including frontotemporal dementia, amyotrophic lateral sclerosis, and Alzheimer's disease. 4 key findings →

Evidence: moderate

Full summary, score breakdown and related studies → Original source Free full text

Genetic contributions to Alzheimer’s disease and frontotemporal dementia in admixed Latin American populations

✓ Peer-reviewed alzhub usefulness score 48 out of 100. npj Dementia 2026-01-21

Latin America’s diverse genetic landscape provides a unique opportunity to study Alzheimer’s disease (AD) and frontotemporal dementia (FTD). 1 key finding →

Participants: 2,162 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Expression of Nrf2 in neurodegenerative diseases

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of neuropathology and experimental neurology 2007-01-01

In response to oxidative stress, the nuclear factor E2-related factor 2 (Nrf2) transcription factor translocates from the cytoplasm into the nucleus and transactivates expression of genes with antioxidant activity. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Proteasomal function is impaired in substantia nigra in Parkinson's disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Neuroscience letters 2001-01-01

The accumulation of alpha-synuclein, ubiquitin and other proteins in Lewy bodies in degenerating dopaminergic neurones in substantia nigra in idiopathic Parkinson's disease (PD) suggest that inhibition of normal/abnormal protein degradation may contribute to neuronal death. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Mutations of tau protein in frontotemporal dementia promote aggregation of paired helical filaments by enhancing local beta-structure

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2001-10-17

The microtubule-associated protein tau is a natively unfolded protein in solution, yet it is able to polymerize into the ordered paired helical filaments (PHF) of Alzheimer's disease. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Global analysis of TDP-43 interacting proteins reveals strong association with RNA splicing and translation machinery

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of proteome research 2010-02-01

TDP-43 is a highly conserved and ubiquitously expressed member of the heterogeneous nuclear ribonucleoprotein (hnRNP) family of proteins. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Progressive increase of frontostriatal brain activation from childhood to adulthood during event-related tasks of cognitive control

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Human brain mapping 2006-12-01

Higher cognitive inhibitory and attention functions have been shown to develop throughout adolescence, presumably concurrent with anatomical brain maturational changes. 1 key finding →

Evidence: high

Full summary, score breakdown and related studies → Original source Free full text

Chaperone-mediated autophagy markers in Parkinson disease brains

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Archives of neurology 2010-08-09

These findings suggest that there is reduced chaperone-mediated autophagy activity in the PD brain, provide evidence for the role of autophagy in PD pathogenesis and Lewy body formation, and suggest that this pathway may be a suitable therapeutic target in PD. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Differential neuropathological alterations in transgenic mice expressing alpha-synuclein from the platelet-derived growth factor and Thy-1 promoters

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of neuroscience research 2002-06-01

Accumulation of alpha-synuclein has been associated with neurodegenerative disorders, such as Lewy body disease and multiple system atrophy. 5 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Patients with amyotrophic lateral sclerosis and other neurodegenerative diseases have increased levels of neurofilament protein in CSF

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Journal of neurochemistry 1996-11-01

In the present study we describe an ELISA to quantify the light subunit of the neurofilament triplet protein (NFL) in CSF. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Neuropathology in mice expressing human alpha-synuclein

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2000-08-01

The presynaptic protein alpha-synuclein is a prime suspect for contributing to Lewy pathology and clinical aspects of diseases, including Parkinson's disease, dementia with Lewy bodies, and a Lewy body variant of Alzheimer's disease. alpha-Synuclein accumulates in Lewy bodies and Lewy neurites, and two missense mutations (A53T and A30P) in the alpha-synuclein gene are genetically linked to rare familial forms of Parkinson's disease. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

VCP/p97 is essential for maturation of ubiquitin-containing autophagosomes and this function is impaired by mutations that cause IBMPFD

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Autophagy 2010-02-22

VCP (VCP/p97) is a ubiquitously expressed member of the AAA(+)-ATPase family of chaperone-like proteins that regulates numerous cellular processes including chromatin decondensation, homotypic membrane fusion and ubiquitin-dependent protein degradation by the proteasome. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Neuropathology provides clues to the pathophysiology of Gaucher disease

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular genetics and metabolism 2004-07-01

To better understand the pathogenesis of brain dysfunction in Gaucher disease (GD), we studied brain pathology in seven subjects with type 1 GD (four also exhibited parkinsonism and dementia), three with type 2 GD and four with type 3 GD. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Full text may need a subscription

Tau filament formation in transgenic mice expressing P301L tau

✓ Peer-reviewed alzhub usefulness score 47 out of 100. The Journal of biological chemistry 2001-01-01

Mutations in the microtubule-associated protein tau, including P301L, are genetically coupled to hereditary frontotemporal dementia with parkinsonism linked to chromosome 17. 3 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Axon pathology in Parkinson's disease and Lewy body dementia hippocampus contains alpha-, beta-, and gamma-synuclein

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Proceedings of the National Academy of Sciences of the United States of America 1999-11-01

Pathogenic alpha-synuclein (alphaS) gene mutations occur in rare familial Parkinson's disease (PD) kindreds, and wild-type alphaS is a major component of Lewy bodies (LBs) in sporadic PD, dementia with LBs (DLB), and the LB variant of Alzheimer's disease, but beta-synuclein (betaS) and gamma-synuclein (gammaS) have not yet been implicated in neurological disorders. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Mitochondrial dysfunction associated with increased oxidative stress and α-synuclein accumulation in PARK2 iPSC-derived neurons and postmortem brain tissue

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular brain 2012-10-06

Pathogenic changes in the brain of a PARK2 patient were recapitulated using iPSC technology. 1 key finding →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

TDP-43 is directed to stress granules by sorbitol, a novel physiological osmotic and oxidative stressor

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Molecular and cellular biology 2010-12-20

TDP-43, or TAR DNA-binding protein 43, is a pathological marker of a spectrum of neurodegenerative disorders, including amyotrophic lateral sclerosis and frontotemporal lobar degeneration with ubiquitin-positive inclusions. 2 key findings →

Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

Neuroimaging and plasma biomarker differences and commonalities in Lewy body dementia subtypes

✓ Peer-reviewed alzhub usefulness score 47 out of 100. Alzheimer s & Dementia 2025-05-01

We show reduced fiber cross-section in LBD versus PD, and increased concentrations of plasma neurofilament light chain and p-tau217; with p-tau217 and fiber cross-section associated with cognition. 5 key findings →

Participants: 47 Evidence: low

Full summary, score breakdown and related studies → Original source Free full text

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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