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Research

28,180 Alzheimer's and dementia studies in plain English, each scored out of 100.

Find studies

Showing 151–175 of 566 studies in Lewy body dementia (page 7 of 23) · 28,180 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; 13,658 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.

Phosphorylation of Ser-129 is the dominant pathological modification of alpha-synuclein in familial and sporadic Lewy body disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. The Journal of biological chemistry 2006-07-17

A comprehensive, unbiased inventory of synuclein forms present in Lewy bodies from patients with dementia with Lewy bodies was carried out using two-dimensional immunoblot analysis, novel sandwich enzyme-linked immunosorbent assays with modification-specific synuclein antibodies, and mass spectroscopy. 1 key finding →

Evidence: low

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

Stress granules and neurodegeneration

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature reviews. Neuroscience 2019-10-03

Recent advances suggest that the response of RNA metabolism to stress has an important role in the pathophysiology of neurodegenerative diseases, particularly amyotrophic lateral sclerosis, frontotemporal dementias and Alzheimer disease. 2 key findings →

Evidence: low

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

S-nitrosylation of parkin regulates ubiquitination and compromises parkin's protective function

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science (New York, N.Y.) 2004-04-22

Parkin is an E3 ubiquitin ligase involved in the ubiquitination of proteins that are important in the survival of dopamine neurons in Parkinson's disease (PD). 4 key findings →

Evidence: low

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

The process of Lewy body formation, rather than simply α-synuclein fibrillization, is one of the major drivers of neurodegeneration

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2020-02-19

Parkinson's disease (PD) is characterized by the accumulation of misfolded and aggregated α-synuclein (α-syn) into intraneuronal inclusions named Lewy bodies (LBs). 1 key finding →

Evidence: low

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

Parkin ubiquitinates the alpha-synuclein-interacting protein, synphilin-1: implications for Lewy-body formation in Parkinson disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature medicine 2001-10-01

Parkinson disease is a common neurodegenerative disorder characterized by the loss of dopaminergic neurons and the presence of intracytoplasmic-ubiquitinated inclusions (Lewy bodies). 3 key findings →

Evidence: low

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

Tar DNA binding protein-43 (TDP-43) associates with stress granules: analysis of cultured cells and pathological brain tissue

✓ Peer-reviewed alzhub usefulness score 55 out of 100. PloS one 2010-10-11

Tar DNA Binding Protein-43 (TDP-43) is a principle component of inclusions in many cases of frontotemporal lobar degeneration (FTLD-U) and amyotrophic lateral sclerosis (ALS). 3 key findings →

Evidence: low

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

Aberrant cleavage of TDP-43 enhances aggregation and cellular toxicity

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Proceedings of the National Academy of Sciences of the United States of America 2009-04-21

Inclusions of TAR DNA-binding protein-43 (TDP-43), a nuclear protein that regulates transcription and RNA splicing, are the defining histopathological feature of frontotemporal lobar degeneration with ubiquitin-positive inclusions (FTLD-Us) and sporadic and familial forms of amyotrophic lateral sclerosis (ALS). 1 key finding →

Evidence: low

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

Functional multivesicular bodies are required for autophagic clearance of protein aggregates associated with neurodegenerative disease

✓ Peer-reviewed alzhub usefulness score 55 out of 100. The Journal of cell biology 2007-11-01

The endosomal sorting complexes required for transport (ESCRTs) are required to sort integral membrane proteins into intralumenal vesicles of the multivesicular body (MVB). 3 key findings →

Evidence: low

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

Clinicopathological and imaging correlates of progressive aphasia and apraxia of speech

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Brain : a journal of neurology 2006-04-13

Apraxia of speech (AOS) is a motor speech disorder characterized by slow speaking rate, abnormal prosody and distorted sound substitutions, additions, repetitions and prolongations, sometimes accompanied by groping, and trial and error articulatory movements. 1 key finding →

Evidence: low

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

Hexanucleotide repeats in ALS/FTD form length-dependent RNA foci, sequester RNA binding proteins, and are neurotoxic

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Cell reports 2013-11-27

The GGGGCC (G4C2) intronic repeat expansion within C9ORF72 is the most common genetic cause of 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

Stress Granule Assembly Disrupts Nucleocytoplasmic Transport

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Cell 2018-04-05

Defects in nucleocytoplasmic transport have been identified as a key pathogenic event in amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD) mediated by a GGGGCC hexanucleotide repeat expansion in C9ORF72, the most common genetic cause of ALS/FTD. 1 key finding →

Evidence: low

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

Lewy bodies and parkinsonism in families with parkin mutations

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Annals of neurology 2001-09-01

Previous work has established that compound mutations and homozygous loss of function of the parkin gene cause early-onset, autosomal recessive parkinsonism. 4 key findings →

Participants: 38 Evidence: low

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

Functional and dynamic polymerization of the ALS-linked protein TDP-43 antagonizes its pathologic aggregation

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Nature communications 2017-06-29

TDP-43 is a primarily nuclear RNA-binding protein, whose abnormal phosphorylation and cytoplasmic aggregation characterizes affected neurons in patients with amyotrophic lateral sclerosis and frontotemporal dementia. 3 key findings →

Evidence: low

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

Profiles of extracellular miRNA in cerebrospinal fluid and serum from patients with Alzheimer's and Parkinson's diseases correlate with disease status and features of pathology

✓ Peer-reviewed alzhub usefulness score 55 out of 100. PloS one 2014-05-05

The discovery and reliable detection of markers for neurodegenerative diseases have been complicated by the inaccessibility of the diseased tissue--such as the inability to biopsy or test tissue from the central nervous system directly. 2 key findings →

Participants: 69 Evidence: low

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

Ubiquitination of G3BP1 mediates stress granule disassembly in a context-specific manner

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science (New York, N.Y.) 2021-06-01

Stress granules are dynamic, reversible condensates composed of RNA and protein that assemble in eukaryotic cells in response to a variety of stressors and are normally disassembled after stress is removed. 2 key findings →

Evidence: low

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

Proteomic analysis reveals distinct cerebrospinal fluid signatures across genetic frontotemporal dementia subtypes

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Science Translational Medicine 2025-02-05

We used an untargeted mass spectrometric approach, tandem mass tag proteomics, for the identification of proteomic signatures in genetic frontotemporal dementia (FTD). 5 key findings →

Participants: 238 Evidence: low

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

Atrophy patterns of deep gray matter nuclei in Alzheimer's disease and frontotemporal dementia

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Journal of Alzheimer s Disease 2025-10-29

BackgroundWhile cortical atrophy has been widely studied in dementia, emerging evidence highlights the role of subcortical degeneration, particularly in deep gray matter structures such as the thalamus, claustrum, and basal nuclei, in both Alzheimer's disease (AD) and frontotemporal dementia (FTD). 3 key findings →

Design: longitudinal study Participants: 380 Evidence: moderate

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

Effect of depression on risks of Alzheimer’s disease and vascular dementia: A real-world longitudinal study

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Psychiatry Research 2025-09-02

During an average follow-up of 3.63 years, we observed a total of 1 493 individuals developing dementia among 4 341 depressed and 43 214 matched non-depressed individuals (62.4% female; mean [SD] age at baseline 64.4 [11.1] years). 5 key findings →

Design: longitudinal study Participants: 493 Evidence: moderate

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

Clinical and neuropathological associations of plasma Aβ42/Aβ40, p‐tau217 and neurofilament light in sporadic frontotemporal dementia spectrum disorders

✓ Peer-reviewed alzhub usefulness score 55 out of 100. Alzheimer s & Dementia Diagnosis Assessment & Disease Monitoring 2025-01-01

Plasma p‐tau217 has clinical, neuroimaging, and neuropathological correlates in sporadic FTD and may identify FTD cases with AD co‐pathology. 1 key finding →

Design: longitudinal study Participants: 620 Evidence: moderate

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

The many faces of α-synuclein: from structure and toxicity to therapeutic target

✓ Peer-reviewed alzhub usefulness score 54 out of 100. Nature reviews. Neuroscience 2013-01-01

Disorders characterized by α-synuclein (α-syn) accumulation, Lewy body formation and parkinsonism (and in some cases dementia) are collectively known as Lewy body diseases. 4 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 28,180 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 28,180 records, built mostly from automated pulls of Europe PMC (61.7% of the library) and OpenAlex (18.1%), 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.

1,034 records (3.7% 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