Zhang Xiangbo, Yu Haiyang, Feng Juan
Department of Neurology, Shengjing Hospital of China Medical University, Shenyang, China.
Front Aging Neurosci. 2024 Oct 9;16:1411104. doi: 10.3389/fnagi.2024.1411104. eCollection 2024.
Parkinson's disease (PD) is the second most common neurodegenerative disease worldwide, significantly prejudicing the health and quality of life of elderly patients. The main pathological characteristics of PD are the loss of dopaminergic neurons in the substantia nigra (SN) as well as abnormal aggregation of α-synuclein (α-syn) monomers and oligomers, which results in formation of Lewy bodies (LBs). Intercellular transmission of α-syn is crucial for PD progression. Microglia play diverse roles in physiological and pathological conditions, exhibiting neuroprotective or neurotoxic effects; moreover, they may directly facilitate α-syn propagation. Various forms of extracellular α-syn can be taken up by microglia through multiple mechanisms, degraded or processed into more pathogenic forms, and eventually released into extracellular fluid or adjacent cells. This review discusses current literature regarding the molecular mechanisms underlying the uptake, degradation, and release of α-syn by microglia.
帕金森病（PD）是全球第二常见的神经退行性疾病，严重损害老年患者的健康和生活质量。PD的主要病理特征是黑质（SN）中多巴胺能神经元的丧失以及α-突触核蛋白（α-syn）单体和寡聚体的异常聚集，这导致路易小体（LBs）的形成。α-syn的细胞间传播对PD的进展至关重要。小胶质细胞在生理和病理条件下发挥多种作用，表现出神经保护或神经毒性作用；此外，它们可能直接促进α-syn的传播。各种形式的细胞外α-syn可以通过多种机制被小胶质细胞摄取，降解或加工成更具致病性的形式，并最终释放到细胞外液或相邻细胞中。本文综述了目前关于小胶质细胞摄取、降解和释放α-syn的分子机制的文献。
