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Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease
Oxidative stress and neuroinflammation are common bases for disease onset and progression in many neurodegenerative diseases. In Parkinson disease, which is characterized by the degeneration of dopaminergic neurons resulting in dopamine depletion, the pathogenesis differs between hereditary and soli...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8773262/ https://www.ncbi.nlm.nih.gov/pubmed/35052674 http://dx.doi.org/10.3390/antiox11010170 |
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author | Takahashi, Shinichi Mashima, Kyoko |
author_facet | Takahashi, Shinichi Mashima, Kyoko |
author_sort | Takahashi, Shinichi |
collection | PubMed |
description | Oxidative stress and neuroinflammation are common bases for disease onset and progression in many neurodegenerative diseases. In Parkinson disease, which is characterized by the degeneration of dopaminergic neurons resulting in dopamine depletion, the pathogenesis differs between hereditary and solitary disease forms and is often unclear. In addition to the pathogenicity of alpha-synuclein as a pathological disease marker, the involvement of dopamine itself and its interactions with glial cells (astrocyte or microglia) have attracted attention. Pacemaking activity, which is a hallmark of dopaminergic neurons, is essential for the homeostatic maintenance of adequate dopamine concentrations in the synaptic cleft, but it imposes a burden on mitochondrial oxidative glucose metabolism, leading to reactive oxygen species production. Astrocytes provide endogenous neuroprotection to the brain by producing and releasing antioxidants in response to oxidative stress. Additionally, the protective function of astrocytes can be modified by microglia. Some types of microglia themselves are thought to exacerbate Parkinson disease by releasing pro-inflammatory factors (M1 microglia). Although these inflammatory microglia may further trigger the inflammatory conversion of astrocytes, microglia may induce astrocytic neuroprotective effects (A2 astrocytes) simultaneously. Interestingly, both astrocytes and microglia express dopamine receptors, which are upregulated in the presence of neuroinflammation. The anti-inflammatory effects of dopamine receptor stimulation are also attracting attention because the functions of astrocytes and microglia are greatly affected by both dopamine depletion and therapeutic dopamine replacement in Parkinson disease. In this review article, we will focus on the antioxidative and anti-inflammatory effects of astrocytes and their synergism with microglia and dopamine. |
format | Online Article Text |
id | pubmed-8773262 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-87732622022-01-21 Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease Takahashi, Shinichi Mashima, Kyoko Antioxidants (Basel) Review Oxidative stress and neuroinflammation are common bases for disease onset and progression in many neurodegenerative diseases. In Parkinson disease, which is characterized by the degeneration of dopaminergic neurons resulting in dopamine depletion, the pathogenesis differs between hereditary and solitary disease forms and is often unclear. In addition to the pathogenicity of alpha-synuclein as a pathological disease marker, the involvement of dopamine itself and its interactions with glial cells (astrocyte or microglia) have attracted attention. Pacemaking activity, which is a hallmark of dopaminergic neurons, is essential for the homeostatic maintenance of adequate dopamine concentrations in the synaptic cleft, but it imposes a burden on mitochondrial oxidative glucose metabolism, leading to reactive oxygen species production. Astrocytes provide endogenous neuroprotection to the brain by producing and releasing antioxidants in response to oxidative stress. Additionally, the protective function of astrocytes can be modified by microglia. Some types of microglia themselves are thought to exacerbate Parkinson disease by releasing pro-inflammatory factors (M1 microglia). Although these inflammatory microglia may further trigger the inflammatory conversion of astrocytes, microglia may induce astrocytic neuroprotective effects (A2 astrocytes) simultaneously. Interestingly, both astrocytes and microglia express dopamine receptors, which are upregulated in the presence of neuroinflammation. The anti-inflammatory effects of dopamine receptor stimulation are also attracting attention because the functions of astrocytes and microglia are greatly affected by both dopamine depletion and therapeutic dopamine replacement in Parkinson disease. In this review article, we will focus on the antioxidative and anti-inflammatory effects of astrocytes and their synergism with microglia and dopamine. MDPI 2022-01-17 /pmc/articles/PMC8773262/ /pubmed/35052674 http://dx.doi.org/10.3390/antiox11010170 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 Takahashi, Shinichi Mashima, Kyoko Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease |
title | Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease |
title_full | Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease |
title_fullStr | Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease |
title_full_unstemmed | Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease |
title_short | Neuroprotection and Disease Modification by Astrocytes and Microglia in Parkinson Disease |
title_sort | neuroprotection and disease modification by astrocytes and microglia in parkinson disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8773262/ https://www.ncbi.nlm.nih.gov/pubmed/35052674 http://dx.doi.org/10.3390/antiox11010170 |
work_keys_str_mv | AT takahashishinichi neuroprotectionanddiseasemodificationbyastrocytesandmicrogliainparkinsondisease AT mashimakyoko neuroprotectionanddiseasemodificationbyastrocytesandmicrogliainparkinsondisease |