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Research models to study lewy body dementia
Suelen Lucio Boschen, Aarushi A. Mukerjee, Ayman H. Faroqi, Benjamin E. Rabichow, John Denis Fryer. Molecular Neurodegeneration, 2025-04-23
Topic: Risk, prevention and care in population studies
Lewy body dementia (LBD) encompasses neurodegenerative dementias characterized by cognitive fluctuations, visual hallucinations, and parkinsonism. Clinical differentiation of LBD from Alzheimer's disease (AD) remains complex due to symptom overlap, yet approximately 25% of dementia cases are diagnosed as LBD postmortem, primarily identified by the presence of α-synuclein aggregates, tau tangles, and amyloid plaques. These pathological features position LBD as a comorbid condition of both Parkinson's disease (PD) and AD, with over 50% of LBD cases exhibiting co-pathologies. LBD's mixed pathology complicates the development of comprehensive models that reflect the full spectrum of LBD's etiological, clinical, and pathological features. While existing animal and cellular models have facilitated significant discoveries in PD and AD research, they lack specificity in capturing LBD's unique pathogenic mechanisms, limiting the exploration of therapeutic avenues for LBD specifically. This review assesses widely used PD and AD models in terms of their relevance to LBD, particularly focusing on their ability to replicate human disease pathology and assess treatment efficacy. Furthermore, we discuss potential modifications to these models to advance the understanding of LBD mechanisms and propose innovative research directions aimed at developing models with enhanced etiological, face, predictive, and construct validity.
Key findings
- While existing animal and cellular models have facilitated significant discoveries in PD and AD research, they lack specificity in capturing LBD's unique pathogenic mechanisms, limiting the exploration of therapeutic avenues for LBD specifically.
Why it matters
Existing animal and cellular models lack specificity in capturing LBD's unique pathogenic mechanisms, limiting the exploration of therapeutic avenues for LBD specifically. This review assesses widely used PD and AD models for their relevance to LBD and discusses potential modifications to advance understanding of LBD mechanisms.
Study details
- Evidence strengthLow
How this study scored 42/100
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.
| Component | Points | Why |
|---|---|---|
| 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 13 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 4.3 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 7.3× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 13 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author John Denis Fryer: h-index 65 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | Mayo Clinic: institution h-index 1,606 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40269912) |
| Free to read | 2 / 2 | Free to read |
| Total | 42 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-025-00837-w
- PubMed: 40269912
- Original source →
- Free full text: Molecular Neurodegeneration →
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
Boschen, S. L., Mukerjee, A. A., Faroqi, A. H., Rabichow, B. E., & Fryer, J. D. (2025). Research models to study lewy body dementia. Molecular Neurodegeneration. https://doi.org/10.1186/s13024-025-00837-w
Vancouver
Boschen SL, Mukerjee AA, Faroqi AH, Rabichow BE, Fryer JD. Research models to study lewy body dementia. Molecular Neurodegeneration. 2025. doi:10.1186/s13024-025-00837-w. PMID: 40269912.
BibTeX
@article{boschen2025-40269912,
author = {Boschen, Suelen Lucio and Mukerjee, Aarushi A. and Faroqi, Ayman H. and Rabichow, Benjamin E. and Fryer, John Denis},
title = {{Research models to study lewy body dementia}},
journal = {Molecular Neurodegeneration},
year = {2025},
doi = {10.1186/s13024-025-00837-w},
pmid = {40269912},
url = {https://doi.org/10.1186/s13024-025-00837-w}
}
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