Abstract：
Alpha-synuclein (α-Syn) is a specific neuronal protein that regulates neurotransmitter release and trafficking of synaptic vesicles. Exosome-associated α-Syn which is specific to the central nervous system (CNS) is involved in the pathogenesis of epilepsy. Therefore, this review aimed to elucidate the possible link between α-Syn and epilepsy, and how it affects the pathophysiology of epilepsy. A neurodegenerative protein such as α-Syn is implicated in the pathogenesis of epilepsy. Evidence from preclinical and clinical studies revealed that upregulation of α-Syn induces progressive neuronal dysfunctions through induction of oxidative stress, neuroinflammation, and inhibition of autophagy in a vicious cycle with subsequent development of severe epilepsy. In addition, accumulation of α-Syn in epilepsy could be secondary to the different cellular alterations including oxidative stress, neuroinflammation, reduction of brain-derived neurotrophic factor (BDNF) and progranulin (PGN), and failure of the autophagy pathway. However, the mechanism of α-Syn-induced-epileptogenesis is not well elucidated. Therefore, α-Syn could be a secondary consequence of epilepsy. Preclinical and clinical studies are warranted to confirm this causal relationship.
摘要：
α-突触核蛋白（α-Syn）是一种特定的神经元蛋白，可调节突触小泡的神经递质释放和运输。外泌体相关的α-Syn是中枢神经系统（CNS）特异性的，与癫痫的发病机理有关。因此,这篇综述旨在阐明α-Syn与癫痫之间的可能联系，以及它如何影响癫痫的病理生理学。神经变性蛋白如α-Syn与癫痫的发病机理有关。来自临床前和临床研究的证据表明，α-Syn的上调通过诱导氧化应激诱导进行性神经元功能障碍，神经炎症，和抑制自噬的恶性循环，随后发展为严重的癫痫。此外,α-Syn在癫痫中的积累可能继发于不同的细胞改变，包括氧化应激，神经炎症，减少脑源性神经营养因子（BDNF）和前颗粒蛋白（PGN），和自噬途径的失败。然而,α-Syn诱导的癫痫发生机制尚不清楚。因此,α-Syn可能是癫痫的次要后果。有必要进行临床前和临床研究以确认这种因果关系。
