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首页|期刊导航|Neural Regeneration Research|The autophagy-lysosome pathway:a potential target in the chemical and gene therapeutic strategies for Parkinson’s disease

The autophagy-lysosome pathway:a potential target in the chemical and gene therapeutic strategies for Parkinson’s diseaseOA

中文摘要

Parkinson’s disease is a common neurodegenerative disease with movement disorders associated with the intracytoplasmic deposition of aggregate proteins such asα-synuclein in neurons.As one of the major intracellular degradation pathways,the autophagy-lysosome pathway plays an important role in eliminating these proteins.Accumulating evidence has shown that upregulation of the autophagy-lysosome pathway may contribute to the clearance ofα-synuclein aggregates and protect against degeneration of dopaminergic neurons in Parkinson’s disease.Moreover,multiple genes associated with the pathogenesis of Parkinson’s disease are intimately linked to alterations in the autophagy-lysosome pathway.Thus,this pathway appears to be a promising therapeutic target for treatment of Parkinson’s disease.In this review,we briefly introduce the machinery of autophagy.Then,we provide a description of the effects of Parkinson’s disease–related genes on the autophagy-lysosome pathway.Finally,we highlight the potential chemical and genetic therapeutic strategies targeting the autophagy–lysosome pathway and their applications in Parkinson’s disease.

Fengjuan Jiao;Lingyan Meng;Kang Du;Xuezhi Li;

School of Mental Health,Jining Medical University,Jining,Shandong Province,China Shandong Collaborative Innovation Center for Diagnosis,Treatment and Behavioral Interventions of Mental Disorders,Institute of Mental Health,Jining Medical University,Jining,Shandong Province,ChinaSchool of Mental Health,Jining Medical University,Jining,Shandong Province,China

临床医学

autophagychemical therapygene therapyParkinson’s diseaseα-synuclein

《Neural Regeneration Research》 2025 (001)

P.139-158 / 20

supported by the National Natural Science Foundation of China,No.82101340(to FJ).

10.4103/NRR.NRR-D-23-01195

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