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5. GBA deficiency promotes SNCA/α-synuclein accumulation through autophagic inhibition by inactivated P

GBA deficiency promotes SNCA/α-synuclein accumulation through autophagic inhibition by inactivated P

来源 :The 6th FAONS Congress and 11th Biennial Conference of CNS(第 | 被引量 : 0次 | 上传用户：gm_686

【摘 要】

：

Objective Loss-of-function mutations in the gene encoding glucocerebrosidase(GBA),the enzyme deficient in the lysosomal storage disorder Gaucher disease,elevate the risk of Parkinsons disease(PD),whic

【作 者】

：

Xue Wang Ting-Ting Du Yong-Quan Lu Chun-Li Duan Hui Yang 

【机 构】

：

Center of Parkinson's Disease Beijing Institute for Brain Disorders,Key Laboratory for Neurodegener

【出 处】

：

The 6th FAONS Congress and 11th Biennial Conference of CNS(第

【发表日期】

：

2015年3期

【关键词】

：

Parkinson's disease (PD) α-synuclein (SNCA) glucocerebrosidase (GBA) protei 

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　　Objective Loss-of-function mutations in the gene encoding glucocerebrosidase(GBA),the enzyme deficient in the lysosomal storage disorder Gaucher disease,elevate the risk of Parkinsons disease(PD),which is characterized by the misprocessing of α-synuclein(SNCA).

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