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This page is alzhub.org's plain-English summary of a published study, not the paper itself. It is generated from the record we hold for this study, sourced and linked below — check the original for the full text and methods.

✓ Peer-reviewed alzhub usefulness score 38 out of 100. Lewy body dementia

Topic: Amyloid, tau and blood-test diagnosis

Lewy body dementia (LBD) is a neurodegenerative disorder characterized by a combination of progressive dementia and spontaneous parkinsonian symptoms. As the second most prevalent form of neurodegenerative dementia after Alzheimer’s disease (AD), LBD necessitates a deeper understanding of its pathogenesis to enable the development of targeted therapeutic interventions. While numerous reviews focus on documenting the clinical manifestations and therapeutic modalities for LBD, animal models provide valuable insights into the underlying mechanisms and potential therapeutic strategies. In this review, we systematically analyze the hallmarks of LBD pathogenesis, genetic risk factors, clinical features, and treatment strategies. Importantly, we emphasize and critically evaluate the pivotal role of animal models in LBD research in advancing our understanding of this disorder, offering a comprehensive framework to elucidate the interactions among misfolded proteins and their role in LBD pathogenesis. Our review proposes new directions for LBD therapeutic management and facilitates the development of innovative pharmacological interventions.

Key findings

Why it matters

This is a review of Lewy body dementia that analyses disease hallmarks, genetic risk factors, clinical features and treatment strategies, and evaluates the role of animal models in this research. It proposes directions for future Lewy body dementia therapeutic management and does not report any treatment, cure or prevention for Alzheimer's disease.

Study details

How this study scored 38/100
How this study's score is builtJournal tier 7 of 10; Journal's citation record 2 of 4; Study design 0 of 12; Strength of evidence 1 of 5; Peer-review validation 10 of 10; How recent 4 of 5; Sample size 0 of 4; Effect reported 0 of 3; Studied in people 0 of 3; Randomised / blinded 0 of 2; Times cited 2 of 7; Citations per year 1 of 5; Impact for its field and year 3 of 6; Cited by studies here 1 of 6; Still being cited 1 of 4; Senior author's track record 1 of 4; Institution's track record 0 of 3; Multi-centre collaboration 1 of 3; Indexed in PubMed 2 of 2; Free to read 2 of 2. Total 38 of 100.38 of 100 points earned62 not earned

Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it.

ComponentPointsWhy
Journal tier 7 / 10 Tier 3 — peer-reviewed journal (Molecular Neurodegeneration)
Journal's citation record 2 / 4 Molecular Neurodegeneration: journal h-index 164 (OpenAlex, 2026-10-29)
Study design 0 / 12 No study design recorded — scores zero, not guessed (not stated in the record — scored 0)
Strength of evidence 1 / 5 Rated “low” in our summary
Peer-review validation 10 / 10 Peer-reviewed. Published as an article in a named peer-reviewed journal.
How recent 4 / 5 2025 — within 3 year(s) of the newest study here
Sample size 0 / 4 Participant count not stated — scores zero (not stated in the record — scored 0)
Effect reported 0 / 3 No effect size reported — scores zero (not stated in the record — scored 0)
Studied in people 0 / 3 Not stated whether this was studied in people — scores zero (not stated in the record — scored 0)
Randomised / blinded 0 / 2 No randomisation or blinding stated — scores zero (not stated in the record — scored 0)
Times cited 2 / 7 Cited 8 times (OpenAlex, 2026-10-10)
Citations per year 1 / 5 2.7 citations a year over 3 year(s) since 2025
Impact for its field and year 3 / 6 Cited 4.5× the average for papers of its field and year (OpenAlex FWCI)
Cited by studies here 1 / 6 Cited by 1 other studies in this library
Still being cited 1 / 4 Cited 8 times in 2024–2026 (2026 still in progress; OpenAlex)
Senior author's track record 1 / 4 Last-listed author Xiaobing Huang: h-index 10 (OpenAlex, whole career)
Institution's track record 0 / 3 University of Macau: institution h-index 369 (OpenAlex)
Multi-centre collaboration 1 / 3 OpenAlex lists 2 institution(s) in 2 countries
Indexed in PubMed 2 / 2 Indexed in PubMed (PMID 40797227)
Free to read 2 / 2 Free to read
Total 38 / 100 —

What each of these 20 components measures, and what this score is not →

Read the original

Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).

Cite this study APA, Vancouver, BibTeX · download .bib or .ris

Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. Check the citation against the original before you use it.

APA 7th

Liang, J., Li, R., Wong, G., & Huang, X. (2025). Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein. Molecular Neurodegeneration. https://doi.org/10.1186/s13024-025-00879-0

Vancouver

Liang J, Li R, Wong G, Huang X. Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein. Molecular Neurodegeneration. 2025. doi:10.1186/s13024-025-00879-0. PMID: 40797227.

BibTeX

@article{liang2025-40797227,
  author  = {Liang, Jingfeng and Li, Rongzhen and Wong, Garry and Huang, Xiaobing},
  title   = {{Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein}},
  journal = {Molecular Neurodegeneration},
  year    = {2025},
  doi     = {10.1186/s13024-025-00879-0},
  pmid    = {40797227},
  url     = {https://doi.org/10.1186/s13024-025-00879-0}
}

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