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Research

29,780 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 226–250 of 566 studies in Lewy body dementia (page 10 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.

Other subjects

Authors

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

Institutions

From OpenAlex; 15,255 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.

Hospice Use Among Medicare Beneficiaries With Parkinson Disease and Dementia With Lewy Bodies

✓ Peer-reviewed alzhub usefulness score 53 out of 100. JAMA Network Open 2025-03-04

Of 11 327 324 Medicare beneficiaries enrolled in hospice between 2010 and 2020 who met eligibility criteria (mean [SD] age, 85.2 [7.5] years; 781 763 [63.0%] female), there were 958 182 (8.4%) with a primary diagnosis of AD, 232 864 (2.1%) with PD, and 49 340 (0.4%) with DLB. 5 key findings →

Design: cohort study Evidence: moderate

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

Intrinsic capacity in patients with dementia with Lewy bodies compared with those with Alzheimer’s disease: A cross-sectional study

✓ Peer-reviewed alzhub usefulness score 53 out of 100. The journal of nutrition health & aging 2025-03-23

A total of 798 patients (154 with probable DLB and 644 with AD) were included, and the mean age was 81.4 years (SD 6.33). 5 key findings →

Design: cross-sectional Participants: 798 Evidence: moderate

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

Semantic dementia. Progressive fluent aphasia with temporal lobe atrophy

✓ Peer-reviewed alzhub usefulness score 53 out of 100. Brain 1992

We report five patients with a stereotyped clinical syndrome characterized by fluent dysphasia with severe anomia, reduced vocabulary and prominent impairment of single-word comprehension, progressing to a stage of virtually complete dissolution of the semantic components of language.

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

Exogenous alpha-synuclein fibrils seed the formation of Lewy body-like intracellular inclusions in cultured cells

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-11-05

Cytoplasmic inclusions containing alpha-synuclein (alpha-Syn) fibrils, referred to as Lewy bodies (LBs), are the signature neuropathological hallmarks of Parkinson's disease (PD). 1 key finding →

Evidence: low

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

Eukaryotic stress granules are cleared by autophagy and Cdc48/VCP function

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Cell 2013-06-01

Stress granules and P bodies are conserved cytoplasmic aggregates of nontranslating messenger ribonucleoprotein complexes (mRNPs) implicated in the regulation of mRNA translation and decay and are related to RNP granules in embryos, neurons, and pathological inclusions in some degenerative diseases. 1 key finding →

Evidence: low

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

C9orf72-mediated ALS and FTD: multiple pathways to disease

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Nature reviews. Neurology 2018-09-01

The discovery that repeat expansions in the C9orf72 gene are a frequent cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) has revolutionized our understanding of these diseases. 1 key finding →

Evidence: low

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

Synthetic tau fibrils mediate transmission of neurofibrillary tangles in a transgenic mouse model of Alzheimer's-like tauopathy

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2013-01-01

Tauopathies, including Alzheimer's disease (AD) and frontotemporal lobar degeneration with tau pathologies, are neurodegenerative diseases characterized by neurofibrillary tangles (NFTs) comprising filamentous tau protein. 1 key finding →

Evidence: low

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

Age-dependent neurofibrillary tangle formation, neuron loss, and memory impairment in a mouse model of human tauopathy (P301L)

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2005-11-01

Here, we describe the generation of a novel transgenic mouse model of human tauopathy. 5 key findings →

Evidence: low

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

TDP-43 mutant transgenic mice develop features of ALS and frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-10-15

Frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS) are neurodegenerative diseases that show considerable clinical and pathologic overlap, with no effective treatments available. 1 key finding →

Evidence: low

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

Lewy body extracts from Parkinson disease brains trigger α-synuclein pathology and neurodegeneration in mice and monkeys

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Annals of neurology 2014-02-18

α-Synuclein species contained in PD-derived LB are pathogenic and have the capacity to initiate a PD-like pathological process, including intracellular and presynaptic accumulations of pathological α-synuclein in different brain areas and slowly progressive axon-initiated dopaminergic nigrostriatal neurodegeneration. 2 key findings →

Evidence: low

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

Beclin 1 gene transfer activates autophagy and ameliorates the neurodegenerative pathology in alpha-synuclein models of Parkinson's and Lewy body diseases

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2009-10-01

Accumulation of the synaptic protein alpha-synuclein (alpha-syn) is a hallmark of Parkinson's disease (PD) and Lewy body disease (LBD), a heterogeneous group of disorders with dementia and parkinsonism, where Alzheimer's disease and PD interact. 2 key findings →

Evidence: low

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

TDP-43 transgenic mice develop spastic paralysis and neuronal inclusions characteristic of ALS and frontotemporal lobar degeneration

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2010-02-03

Neuronal cytoplasmic and intranuclear aggregates of RNA-binding protein TDP-43 are a hallmark feature of neurodegenerative diseases such as amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). 2 key findings →

Evidence: low

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

Parkin mediates nonclassical, proteasomal-independent ubiquitination of synphilin-1: implications for Lewy body formation

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of neuroscience : the official journal of the Society for Neuroscience 2005-02-01

It is widely accepted that the familial Parkinson's disease (PD)-linked gene product, parkin, functions as a ubiquitin ligase involved in protein turnover via the ubiquitin-proteasome system. 4 key findings →

Evidence: low

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

Antisense proline-arginine RAN dipeptides linked to C9ORF72-ALS/FTD form toxic nuclear aggregates that initiate in vitro and in vivo neuronal death

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Neuron 2014-12-01

Expanded GGGGCC (G4C2) nucleotide repeats within the C9ORF72 gene are the most common genetic mutation associated with both amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). 1 key finding →

Evidence: low

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

Small misfolded Tau species are internalized via bulk endocytosis and anterogradely and retrogradely transported in neurons

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of biological chemistry 2012-11-27

The accumulation of Tau into aggregates is associated with key pathological events in frontotemporal lobe degeneration (FTD-Tau) and Alzheimer disease (AD). 3 key findings →

Evidence: low

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

Molecular determinants and genetic modifiers of aggregation and toxicity for the ALS disease protein FUS/TLS

✓ Peer-reviewed alzhub usefulness score 52 out of 100. PLoS biology 2011-04-26

TDP-43 and FUS are RNA-binding proteins that form cytoplasmic inclusions in some forms of amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD). 1 key finding →

Evidence: low

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

C9ORF72, implicated in amytrophic lateral sclerosis and frontotemporal dementia, regulates endosomal trafficking

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Human molecular genetics 2014-02-18

Intronic expansion of a hexanucleotide GGGGCC repeat in the chromosome 9 open reading frame 72 (C9ORF72) gene is the major cause of familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia. 1 key finding →

Evidence: low

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

Dysregulation of the ALS-associated gene TDP-43 leads to neuronal death and degeneration in mice

✓ Peer-reviewed alzhub usefulness score 52 out of 100. The Journal of clinical investigation 2011-01-04

Amyotrophic lateral sclerosis (ALS) and frontotemporal lobar degeneration (FTLD) are characterized by cytoplasmic protein aggregates in the brain and spinal cord that include TAR-DNA binding protein 43 (TDP-43). 3 key findings →

Evidence: low

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

Organelle-specific autophagy in inflammatory diseases: a potential therapeutic target underlying the quality control of multiple organelles

✓ Peer-reviewed alzhub usefulness score 52 out of 100. Autophagy 2020-02-12

Organelle-specific autophagy is one of the major subtypes of autophagy, selectively targeting different organelles for quality control. 5 key findings →

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 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