Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein
- PMID: 40797227
- PMCID: PMC12345100
- DOI: 10.1186/s13024-025-00879-0
Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein
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.
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.
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References
-
- Stevens T, Livingston G, Kitchen G, Manela M, Walker Z, Katona C. Islington study of dementia subtypes in the community. Br J Psychiatry. 2002;180:270–6. - PubMed
-
- Kosaka K, Yoshimura M, Ikeda K, Budka H. Diffuse type of Lewy body disease: progressive dementia with abundant cortical Lewy bodies and senile changes of varying degree–a new disease? Clin Neuropathol. 1984;3(5):185–92. - PubMed
-
- Goedert M, Spillantini MG, Del Tredici K, Braak H. 100 years of Lewy pathology. Nat Rev Neurol. 2013;9(1):13–24. - PubMed
-
- Matsui Y, Tanizaki Y, Arima H, Yonemoto K, Doi Y, Ninomiya T, et al. Incidence and survival of dementia in a general population of Japanese elderly: the Hisayama study. J Neurol Neurosurg Psychiatry. 2009;80(4):366–70. - PubMed
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