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Cells
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Autophagy in Parkinson's Disease
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Autophagy in Parkinson's Disease

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Autophagy".

Deadline for manuscript submissions: closed (1 September 2023) | Viewed by 9478

Special Issue Editor

Dr. Cristine Alves Da Costa

E-Mail Website
Guest Editor
Institut de Pharmacologie Moléculaire et Cellulaire, Université Côte d'Azur, INSERM, CNRS, IPMC, Valbonne, France
Interests: Parkinson’s disease; Alzheimer’s disease, brain tumors; transcription; autophagy; cell death; ER-stress/unfolded protein response
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Parkinson’s syndrome is a multi-causal and age-related motor disease, the etiology of which as well as cellular and molecular dysfunctional mechanisms are not yet fully elucidated.  Parkinson’s disease (PD) involves the dysregulations of various key cellular processes amongst which the non-lysosomal degradation of proteins by autophagy. Autophagy is a generic term that covers a complex set of processes corresponding to distinct specialized sub-types of autophagy including macroautophagy, microautophagy, and chaperone-mediated autophagy (CMA). Macroautophagy and CMA are at the gravity center of PD pathology and, notably a specific form of macroautophagy, referred to as mitophagy.

The focus of this special issue is to provide the scientific community (neuroscientists, clinicians) interested in PD neurobiology and beyond, with an overview of the current knowledge on the molecular mechanisms underlying autophagy in physiological and PD conditions. I anticipate that this special issue will catch the interest of scientists with various expertise from bench to bedside and gather the most recent advances at the frontline of this cutting-edge field of research in PD.

Dr. Cristine Alves Da Costa
Guest Editor

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Keywords

  • Parkinson’s disease
  • macroautophagy
  • CMA
  • mitophagy
  • reticuphagy
  • PD genes
  • preclinical studies
  • PD neurotoxins
  • therapeutic

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Published Papers (3 papers)

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Research

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26 pages, 8216 KiB  
Article
Syringin Prevents 6-Hydroxydopamine Neurotoxicity by Mediating the MiR-34a/SIRT1/Beclin-1 Pathway and Activating Autophagy in SH-SY5Y Cells and the Caenorhabditis elegans Model
by Ru-Huei Fu, Syuan-Yu Hong and Hui-Jye Chen
Cells 2023, 12(18), 2310; https://doi.org/10.3390/cells12182310 - 19 Sep 2023
Cited by 2 | Viewed by 1885
Abstract
Defective autophagy is one of the cellular hallmarks of Parkinson’s disease (PD). Therefore, a therapeutic strategy could be a modest enhancement of autophagic activity in dopamine (DA) neurons to deal with the clearance of damaged mitochondria and abnormal protein aggregates. Syringin (SRG) is [...] Read more.
Defective autophagy is one of the cellular hallmarks of Parkinson’s disease (PD). Therefore, a therapeutic strategy could be a modest enhancement of autophagic activity in dopamine (DA) neurons to deal with the clearance of damaged mitochondria and abnormal protein aggregates. Syringin (SRG) is a phenolic glycoside derived from the root of Acanthopanax senticosus. It has antioxidant, anti-apoptotic, and anti-inflammatory properties. However, whether it has a preventive effect on PD remains unclear. The present study found that SRG reversed the increase in intracellular ROS-caused apoptosis in SH-SY5Y cells induced by neurotoxin 6-OHDA exposure. Likewise, in C. elegans, degeneration of DA neurons, DA-related food-sensitive behaviors, longevity, and accumulation of α-synuclein were also improved. Studies of neuroprotective mechanisms have shown that SRG can reverse the suppressed expression of SIRT1, Beclin-1, and other autophagy markers in 6-OHDA-exposed cells. Thus, these enhanced the formation of autophagic vacuoles and autophagy activity. This protective effect can be blocked by pretreatment with wortmannin (an autophagosome formation blocker) and bafilomycin A1 (an autophagosome–lysosome fusion blocker). In addition, 6-OHDA increases the acetylation of Beclin-1, leading to its inactivation. SRG can induce the expression of SIRT1 and promote the deacetylation of Beclin-1. Finally, we found that SRG reduced the 6-OHDA-induced expression of miR-34a targeting SIRT1. The overexpression of miR-34a mimic abolishes the neuroprotective ability of SRG. In conclusion, SRG induces autophagy via partially regulating the miR-34a/SIRT1/Beclin-1 axis to prevent 6-OHDA-induced apoptosis and α-synuclein accumulation. SRG has the opportunity to be established as a candidate agent for the prevention and cure of PD. Full article
(This article belongs to the Special Issue Autophagy in Parkinson's Disease)
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19 pages, 4103 KiB  
Article
Systematic Functional Analysis of PINK1 and PRKN Coding Variants
by Benjamin J. Broadway, Paige K. Boneski, Jenny M. Bredenberg, Ana Kolicheski, Xu Hou, Alexandra I. Soto-Beasley, Owen A. Ross, Wolfdieter Springer and Fabienne C. Fiesel
Cells 2022, 11(15), 2426; https://doi.org/10.3390/cells11152426 - 5 Aug 2022
Cited by 12 | Viewed by 3183
Abstract
Loss of either PINK1 or PRKN causes an early onset Parkinson’s disease (PD) phenotype. Functionally, PINK1 and PRKN work together to mediate stress-activated mitochondrial quality control. Upon mitochondrial damage, PINK1, a ubiquitin kinase and PRKN, a ubiquitin ligase, decorate damaged organelles with phosphorylated [...] Read more.
Loss of either PINK1 or PRKN causes an early onset Parkinson’s disease (PD) phenotype. Functionally, PINK1 and PRKN work together to mediate stress-activated mitochondrial quality control. Upon mitochondrial damage, PINK1, a ubiquitin kinase and PRKN, a ubiquitin ligase, decorate damaged organelles with phosphorylated ubiquitin for sequestration and degradation in lysosomes, a process known as mitophagy. While several genetic mutations are established to result in loss of mitophagy function, many others have not been extensively characterized and are of unknown significance. Here, we analyzed a set of twenty variants, ten in each gene, focusing on understudied variants mostly from the Parkinson’s progressive marker initiative, with sensitive assays to define potential functional deficits. Our results nominate specific rare genetic PINK1 and PRKN variants that cause loss of enzymatic function in line with a potential causative role for PD. Additionally, we identify several variants with intermediate phenotypes and follow up on two of them by gene editing midbrain-derived neuronal precursor cells. Thereof derived isogenic neurons show a stability defect of the rare PINK1 D525N mutation, while the common PINK1 Q115L substitution results in reduced kinase activity. Our strategy to analyze variants with sensitive functional readouts will help aid diagnostics and disease treatment in line with current genomic and therapeutic advances. Full article
(This article belongs to the Special Issue Autophagy in Parkinson's Disease)
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Review

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18 pages, 7497 KiB  
Review
Pathogenic Aspects and Therapeutic Avenues of Autophagy in Parkinson’s Disease
by Rémi Kinet and Benjamin Dehay
Cells 2023, 12(4), 621; https://doi.org/10.3390/cells12040621 - 15 Feb 2023
Cited by 8 | Viewed by 3715
Abstract
The progressive aging of the population and the fact that Parkinson’s disease currently does not have any curative treatment turn out to be essential issues in the following years, where research has to play a critical role in developing therapy. Understanding this neurodegenerative [...] Read more.
The progressive aging of the population and the fact that Parkinson’s disease currently does not have any curative treatment turn out to be essential issues in the following years, where research has to play a critical role in developing therapy. Understanding this neurodegenerative disorder keeps advancing, proving the discovery of new pathogenesis-related genes through genome-wide association analysis. Furthermore, the understanding of its close link with the disruption of autophagy mechanisms in the last few years permits the elaboration of new animal models mimicking, through multiple pathways, different aspects of autophagic dysregulation, with the presence of pathological hallmarks, in brain regions affected by Parkinson’s disease. The synergic advances in these fields permit the elaboration of multiple therapeutic strategies for restoring autophagy activity. This review discusses the features of Parkinson’s disease, the autophagy mechanisms and their involvement in pathogenesis, and the current methods to correct this cellular pathway, from the development of animal models to the potentially curative treatments in the preclinical and clinical phase studies, which are the hope for patients who do not currently have any curative treatment. Full article
(This article belongs to the Special Issue Autophagy in Parkinson's Disease)
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