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 i...
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| Format: | Article |
| Language: | English |
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BMC
2025-08-01
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| Series: | Molecular Neurodegeneration |
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| Online Access: | https://doi.org/10.1186/s13024-025-00879-0 |
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| author | Jingfeng Liang Rongzhen Li Garry Wong Xiaobing Huang |
| author_facet | Jingfeng Liang Rongzhen Li Garry Wong Xiaobing Huang |
| author_sort | Jingfeng Liang |
| collection | DOAJ |
| description | 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. |
| format | Article |
| id | doaj-art-ea6b0885a07b44d4b51fb4a88b53fdaa |
| institution | Kabale University |
| issn | 1750-1326 |
| language | English |
| publishDate | 2025-08-01 |
| publisher | BMC |
| record_format | Article |
| series | Molecular Neurodegeneration |
| spelling | doaj-art-ea6b0885a07b44d4b51fb4a88b53fdaa2025-08-20T04:02:41ZengBMCMolecular Neurodegeneration1750-13262025-08-0120112710.1186/s13024-025-00879-0Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synucleinJingfeng Liang0Rongzhen Li1Garry Wong2Xiaobing Huang3College of Pharmacy, Shenzhen Technology UniversityDepartment of Global Public Health and Medicinal Administration, Faculty of Health Sciences, University of MacauDepartment of Global Public Health and Medicinal Administration, Faculty of Health Sciences, University of MacauCollege of Pharmacy, Shenzhen Technology UniversityAbstract 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.https://doi.org/10.1186/s13024-025-00879-0Lewy body dementiaDementia with Lewy bodiesParkinson’s disease dementiaAmyloid βTauΑ-synuclein |
| spellingShingle | Jingfeng Liang Rongzhen Li Garry Wong Xiaobing Huang Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein Molecular Neurodegeneration Lewy body dementia Dementia with Lewy bodies Parkinson’s disease dementia Amyloid β Tau Α-synuclein |
| title | Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein |
| title_full | Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein |
| title_fullStr | Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein |
| title_full_unstemmed | Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein |
| title_short | Lewy body dementia: exploring biomarkers and pathogenic interactions of amyloid β, tau, and α-synuclein |
| title_sort | lewy body dementia exploring biomarkers and pathogenic interactions of amyloid β tau and α synuclein |
| topic | Lewy body dementia Dementia with Lewy bodies Parkinson’s disease dementia Amyloid β Tau Α-synuclein |
| url | https://doi.org/10.1186/s13024-025-00879-0 |
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