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Review
. 2025 Aug 12;20(1):90.
doi: 10.1186/s13024-025-00879-0.

Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein

Affiliations
Review

Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein

Jingfeng Liang et al. Mol Neurodegener. .

Abstract

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.

Keywords: Amyloid β; Dementia with Lewy bodies; Lewy body dementia; Parkinson’s disease dementia; Tau; Α-synuclein.

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Conflict of interest statement

Declarations. Ethics approval and consent to participate: Not applicable. Consent for publication: Not applicable. Competing interests: The authors declare that there are no competing interests.

Figures

Fig. 1
Fig. 1
The pathogenesis hallmarks of LBD
Fig. 2
Fig. 2
Genetic risk factors contribute to the pathogenesis of LBD

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