Dear Editor,

Parkinson’s disease (PD) is a progressive neurodegenerative disorder, which manifests through the abnormal accumulation of pathological amyloid fibrils composed of α-synuclein (α-syn) into Lewy bodies and the deterioration of dopaminergic neurons in the substantia nigra.^1,2,3,4 In addition to α-syn fibrillar aggregation, the disruption of selective autophagy is also tightly linked to the pathogenesis of PD.^5,6 The co-localization of LC3B, the key autophagosome protein in selective autophagy,⁷ and α-syn in the Lewy bodies of PD patients’ brains points towards a potential role of α-syn in modulating selective autophagy.⁸ Yet, the interplay between them has not been mechanistically elucidated.

 亲爱的编辑，

帕金森病（PD）是一种进行性神经退行性疾病，表现为由α-突触核蛋白（α-syn）组成的病理性淀粉样原纤维异常堆积到路易体中以及黑质中多巴胺能神经元的退化。 ^1,2,3,4除了 α-syn 纤维聚集之外，选择性自噬的破坏也与 PD 的发病机制密切相关。 ^5,6 LC3B（选择性自噬中的关键自噬体蛋白） ⁷和 α-syn 在 PD 患者大脑路易体中的共定位表明 α-syn 在调节选择性自噬中具有潜在作用。 ⁸然而，它们之间的相互作用尚未得到机械阐明。