Autophagy in Parkinson’s Disease

Lior Nechushtai, Dan Frenkel, Ronit Pinkas-Kramarski*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

6 Scopus citations

Abstract

Parkinson’s disease (PD) is a devastating disease associated with accumulation of α-synuclein (α-Syn) within dopaminergic neurons, leading to neuronal death. PD is characterized by both motor and non-motor clinical symptoms. Several studies indicate that autophagy, an important intracellular degradation pathway, may be involved in different neurodegenerative diseases including PD. The autophagic process mediates the degradation of protein aggregates, damaged and unneeded proteins, and organelles, allowing their clearance, and thereby maintaining cell homeostasis. Impaired autophagy may cause the accumulation of abnormal proteins. Incomplete or impaired autophagy may explain the neurotoxic accumulation of protein aggregates in several neurodegenerative diseases including PD. Indeed, studies have suggested the contribution of impaired autophagy to α-Syn accumulation, the death of dopaminergic neurons, and neuroinflammation. In this review, we summarize the recent literature on the involvement of autophagy in PD pathogenesis.

Original languageEnglish
Article number1435
JournalBiomolecules
Volume13
Issue number10
DOIs
StatePublished - Oct 2023

Funding

FundersFunder number
Aufzien Center for Prevention and Treatment of Parkinson’s Disease
Prajs-Drimmer Institute for the Development of Anti-Degenerative Drugs
Prajs-Drimmer Institute for the Development of Anti-Degenerative Drugs and Aufzien Family Center for the Prevention and Treatment of Parkinson’s Disease
Association of Pediatric Program Directors
Tel Aviv University

    Keywords

    • Parkinson’s disease (PD)
    • apolipoprotein E4 (apoE4)
    • autophagy
    • endocytosis
    • endocytosis
    • lysosomal degradation
    • synuclein α

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