目前将α -共核蛋白 (α -synuclein)异常积聚所参与引起的神经系统变性病统称为共核蛋白病 (synucle inopathy) ,包括Alzheimer病 (AD)、肌萎缩侧索硬化 (ALS)、帕金森病 (PD)、多系统萎缩 (MSA)和路易体痴呆(DLB)等。研究α -共核蛋白的分子病理机制 ,及其在体与离体情况下与其他物质的相互作用 ,无疑会对某些神经变性疾病发病机制的认识及治疗产生深远的影响 Currently, neurodegenerative diseases caused by the abnormal accumulation of α-synuclein are collectively referred to as synucleinopathy, including Alzheimer’s disease (AD), amyotrophic lateral sclerosis (ALS) (PD), multiple system atrophy (MSA) and dementia with Lewy bodies (DLB). Studying the molecular pathological mechanism of α-synuclein and its interaction with other substances in vitro and in vivo will undoubtedly have a far-reaching impact on the understanding and treatment of the pathogenesis of certain neurodegenerative diseases