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A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology

Parkinson’s disease (PD) is an incurable neurodegenerative disease of high prevalence, characterized by the prominent death of dopaminergic neurons in the substantia nigra pars compacta, which produces dopamine deficiency, leading to classic motor symptoms. Although PD has traditionally been conside...

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Detalles Bibliográficos
Autores principales: Prunell, Giselle, Olivera-Bravo, Silvia
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9775515/
https://www.ncbi.nlm.nih.gov/pubmed/36551173
http://dx.doi.org/10.3390/biom12121745
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author Prunell, Giselle
Olivera-Bravo, Silvia
author_facet Prunell, Giselle
Olivera-Bravo, Silvia
author_sort Prunell, Giselle
collection PubMed
description Parkinson’s disease (PD) is an incurable neurodegenerative disease of high prevalence, characterized by the prominent death of dopaminergic neurons in the substantia nigra pars compacta, which produces dopamine deficiency, leading to classic motor symptoms. Although PD has traditionally been considered as a neuronal cell autonomous pathology, in which the damage of vulnerable neurons is responsible for the disease, growing evidence strongly suggests that astrocytes might have an active role in the neurodegeneration observed. In the present review, we discuss several studies evidencing astrocyte implications in PD, highlighting the consequences of both the loss of normal homeostatic functions and the gain in toxic functions for the wellbeing of dopaminergic neurons. The revised information provides significant evidence that allows astrocytes to be positioned as crucial players in PD etiology, a factor that needs to be taken into account when considering therapeutic targets for the treatment of the disease.
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spelling pubmed-97755152022-12-23 A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology Prunell, Giselle Olivera-Bravo, Silvia Biomolecules Review Parkinson’s disease (PD) is an incurable neurodegenerative disease of high prevalence, characterized by the prominent death of dopaminergic neurons in the substantia nigra pars compacta, which produces dopamine deficiency, leading to classic motor symptoms. Although PD has traditionally been considered as a neuronal cell autonomous pathology, in which the damage of vulnerable neurons is responsible for the disease, growing evidence strongly suggests that astrocytes might have an active role in the neurodegeneration observed. In the present review, we discuss several studies evidencing astrocyte implications in PD, highlighting the consequences of both the loss of normal homeostatic functions and the gain in toxic functions for the wellbeing of dopaminergic neurons. The revised information provides significant evidence that allows astrocytes to be positioned as crucial players in PD etiology, a factor that needs to be taken into account when considering therapeutic targets for the treatment of the disease. MDPI 2022-11-24 /pmc/articles/PMC9775515/ /pubmed/36551173 http://dx.doi.org/10.3390/biom12121745 Text en © 2022 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Prunell, Giselle
Olivera-Bravo, Silvia
A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology
title A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology
title_full A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology
title_fullStr A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology
title_full_unstemmed A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology
title_short A Focus on Astrocyte Contribution to Parkinson’s Disease Etiology
title_sort focus on astrocyte contribution to parkinson’s disease etiology
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9775515/
https://www.ncbi.nlm.nih.gov/pubmed/36551173
http://dx.doi.org/10.3390/biom12121745
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