An update on cellular and molecular determinants of Parkinson's disease with emphasis on the role of the retromer complex.
Parkinson's disease
Vps35
autophagy
dopaminergic neuron
lysosomal dysfunction
mitochondria
neurodegeneration
recycling endosome
retromer complex
trans-Golgi network
Journal
Journal of neuroscience research
ISSN: 1097-4547
Titre abrégé: J Neurosci Res
Pays: United States
ID NLM: 7600111
Informations de publication
Date de publication:
01 2021
01 2021
Historique:
received:
21
12
2019
revised:
25
05
2020
accepted:
26
05
2020
pubmed:
8
7
2020
medline:
3
11
2021
entrez:
8
7
2020
Statut:
ppublish
Résumé
Parkinson's disease (PD) is a highly prevalent neurodegenerative condition. The disease involves the progressive degeneration of dopaminergic neurons located in the substantia nigra pars compacta. Among late-onset, familial forms of Parkinson are cases with mutations in the PARK17 locus encoding the vacuolar protein sorting 35 (Vps35), a subunit of the retromer complex. The retromer complex is composed of a heterotrimeric protein core (Vps26-Vps35-Vps29). The best-known role of retromer is the retrieval of cargoes from endosomes to the Golgi complex or the plasma membrane. However, recent literature indicates that retromer performs roles associated with lysosomal and mitochondrial functions and degradative pathways such as autophagy. A common point mutation affecting the retromer subunit Vps35 is D620N, which has been linked to the alterations in the aforementioned cellular processes as well as with neurodegeneration. Here, we review the main aspects of the malfunction of the retromer complex and its implications for PD pathology. Besides, we highlight several controversies still awaiting clarification.
Substances chimiques
VPS35 protein, human
0
Vesicular Transport Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
163-179Informations de copyright
© 2020 Wiley Periodicals LLC.
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