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Current strategies in the management of dementia with lewy bodies and future directions based on disease pathophysiology
Daniel Erskine, John‐Paul Taylor. Molecular Neurodegeneration, 2025-07-01
Topic: Risk, prevention and care in population studies
Dementia with Lewy bodies (DLB) is thought to be the second most common form of dementia after Alzheimer’s disease, and is characterised by a combination of cognitive, neuropsychiatric and motor symptoms. The present review seeks to discuss current strategies for the management of DLB, and future directions for novel disease-modifying therapies. Current best practice for the clinical management of DLB is based upon therapies that target specific symptom domains due to the lack of disease-modifying therapies. Cholinesterase inhibitors are the frontline treatment for treating cognitive decline in DLB, whereas the treatment of motor symptoms remains challenging due to poor response to dopaminergic therapies and the potential for exacerbation of neuropsychiatric features. There is emerging evidence suggesting a range of further pharmacological and non-pharmacological therapies may be effective in treating specific symptom domains of DLB, but further evidence is warranted to demonstrate their efficacy. A key challenge in the treatment of DLB is incomplete understanding of disease pathophysiology, which has limited attempts to develop disease-modifying therapies. In the present article, we discuss the multi-faceted nature of DLB neuropathology, from Lewy body pathology to mitochondrial dysfunction, and discuss therapies in development that target particular aspects of DLB neuropathology. In particular, we highlight antibody-based therapies to attenuate protein aggregation, compounds that enhance the generation of cellular energy and autophagy-enhancing agents as particular areas of promise. Furthermore, we discuss how optimal strategies for disease modification will be centred on agents that treat DLB neuropathology more holistically, and will be underpinned by a more complete understanding of the pathogenic events that underlie the full spectrum of pathological changes observed in the DLB brain.
Key findings
- There is emerging evidence suggesting a range of further pharmacological and non-pharmacological therapies may be effective in treating specific symptom domains of DLB, but further evidence is warranted to demonstrate their efficacy.
- A key challenge in the treatment of DLB is incomplete understanding of disease pathophysiology, which has limited attempts to develop disease-modifying therapies.
- In the present article, we discuss the multi-faceted nature of DLB neuropathology, from Lewy body pathology to mitochondrial dysfunction, and discuss therapies in development that target particular aspects of DLB neuropathology.
- In particular, we highlight antibody-based therapies to attenuate protein aggregation, compounds that enhance the generation of cellular energy and autophagy-enhancing agents as particular areas of promise.
- Furthermore, we discuss how optimal strategies for disease modification will be centred on agents that treat DLB neuropathology more holistically, and will be underpinned by a more complete understanding of the pathogenic events that underlie the full spectrum of pathological changes observed in the DLB brain.
Why it matters
This review discusses current management strategies for dementia with Lewy bodies, noting that cholinesterase inhibitors are frontline for cognitive decline and that no disease-modifying therapies exist. It highlights emerging evidence for other therapies but states further evidence is needed, so no cure or prevention is available.
Study details
- Evidence strengthLow
How this study scored 41/100
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 10 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 3.3 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 3 / 6 | Cited 5.6× 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 10 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 3 / 4 | Last-listed author John‐Paul Taylor: h-index 67 (OpenAlex, whole career) |
| Institution's track record | 1 / 3 | Newcastle University: institution h-index 932 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 40598239) |
| Free to read | 2 / 2 | Free to read |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1186/s13024-025-00856-7
- PubMed: 40598239
- 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
Erskine, D., & Taylor, J. (2025). Current strategies in the management of dementia with lewy bodies and future directions based on disease pathophysiology. Molecular Neurodegeneration. https://doi.org/10.1186/s13024-025-00856-7
Vancouver
Erskine D, Taylor J. Current strategies in the management of dementia with lewy bodies and future directions based on disease pathophysiology. Molecular Neurodegeneration. 2025. doi:10.1186/s13024-025-00856-7. PMID: 40598239.
BibTeX
@article{erskine2025-40598239,
author = {Erskine, Daniel and Taylor, John‐Paul},
title = {{Current strategies in the management of dementia with lewy bodies and future directions based on disease pathophysiology}},
journal = {Molecular Neurodegeneration},
year = {2025},
doi = {10.1186/s13024-025-00856-7},
pmid = {40598239},
url = {https://doi.org/10.1186/s13024-025-00856-7}
}
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