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Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson’s Disease
Astrocytes are the most abundant neuron-supporting glial cells in the central nervous system. The neuroprotective role of astrocytes has been demonstrated in various neurological disorders such as amyotrophic lateral sclerosis, spinal cord injury, stroke and Parkinson’s disease (PD). Astrocyte dysfu...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Bentham Science Publishers
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4997990/ https://www.ncbi.nlm.nih.gov/pubmed/26795196 http://dx.doi.org/10.2174/0929867323666160122115057 |
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author | Miyazaki, Ikuko Asanuma, Masato |
author_facet | Miyazaki, Ikuko Asanuma, Masato |
author_sort | Miyazaki, Ikuko |
collection | PubMed |
description | Astrocytes are the most abundant neuron-supporting glial cells in the central nervous system. The neuroprotective role of astrocytes has been demonstrated in various neurological disorders such as amyotrophic lateral sclerosis, spinal cord injury, stroke and Parkinson’s disease (PD). Astrocyte dysfunction or loss-of-astrocytes increases the susceptibility of neurons to cell death, while astrocyte transplantation in animal studies has therapeutic advantage. We reported recently that stimulation of serotonin 1A (5-HT(1A)) receptors on astrocytes promoted astrocyte proliferation and upregulated antioxidative molecules to act as a neuroprotectant in parkinsonian mice. PD is a progressive neurodegenerative disease with motor symptoms such as tremor, bradykinesia, rigidity and postural instability, that are based on selective loss of nigrostriatal dopaminergic neurons, and with non-motor symptoms such as orthostatic hypotension and constipation based on peripheral neurodegeneration. Although dopaminergic therapy for managing the motor disability associated with PD is being assessed at present, the main challenge remains the development of neuroprotective or disease-modifying treatments. Therefore, it is desirable to find treatments that can reduce the progression of dopaminergic cell death. In this article, we summarize first the neuroprotective properties of astrocytes targeting certain molecules related to PD. Next, we review neuroprotective effects induced by stimulation of 5-HT(1A) receptors on astrocytes. The review discusses new promising therapeutic strategies based on neuroprotection against oxidative stress and prevention of dopaminergic neurodegeneration. |
format | Online Article Text |
id | pubmed-4997990 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Bentham Science Publishers |
record_format | MEDLINE/PubMed |
spelling | pubmed-49979902016-08-31 Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson’s Disease Miyazaki, Ikuko Asanuma, Masato Curr Med Chem Article Astrocytes are the most abundant neuron-supporting glial cells in the central nervous system. The neuroprotective role of astrocytes has been demonstrated in various neurological disorders such as amyotrophic lateral sclerosis, spinal cord injury, stroke and Parkinson’s disease (PD). Astrocyte dysfunction or loss-of-astrocytes increases the susceptibility of neurons to cell death, while astrocyte transplantation in animal studies has therapeutic advantage. We reported recently that stimulation of serotonin 1A (5-HT(1A)) receptors on astrocytes promoted astrocyte proliferation and upregulated antioxidative molecules to act as a neuroprotectant in parkinsonian mice. PD is a progressive neurodegenerative disease with motor symptoms such as tremor, bradykinesia, rigidity and postural instability, that are based on selective loss of nigrostriatal dopaminergic neurons, and with non-motor symptoms such as orthostatic hypotension and constipation based on peripheral neurodegeneration. Although dopaminergic therapy for managing the motor disability associated with PD is being assessed at present, the main challenge remains the development of neuroprotective or disease-modifying treatments. Therefore, it is desirable to find treatments that can reduce the progression of dopaminergic cell death. In this article, we summarize first the neuroprotective properties of astrocytes targeting certain molecules related to PD. Next, we review neuroprotective effects induced by stimulation of 5-HT(1A) receptors on astrocytes. The review discusses new promising therapeutic strategies based on neuroprotection against oxidative stress and prevention of dopaminergic neurodegeneration. Bentham Science Publishers 2016-03 2016-03 /pmc/articles/PMC4997990/ /pubmed/26795196 http://dx.doi.org/10.2174/0929867323666160122115057 Text en © 2016 Bentham Science Publishers https://creativecommons.org/licenses/by-nc/4.0/legalcode This is an open access article licensed under the terms of the Creative Commons Attribution-Non-Commercial 4.0 International Public License (CC BY-NC 4.0) ( https://creativecommons.org/licenses/by-nc/4.0/legalcode ), which permits unrestricted, non-commercial use, distribution and reproduction in any medium, provided the work is properly cited. |
spellingShingle | Article Miyazaki, Ikuko Asanuma, Masato Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson’s Disease |
title | Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson’s Disease |
title_full | Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson’s Disease |
title_fullStr | Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson’s Disease |
title_full_unstemmed | Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson’s Disease |
title_short | Serotonin 1A Receptors on Astrocytes as a Potential Target for the Treatment of Parkinson’s Disease |
title_sort | serotonin 1a receptors on astrocytes as a potential target for the treatment of parkinson’s disease |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4997990/ https://www.ncbi.nlm.nih.gov/pubmed/26795196 http://dx.doi.org/10.2174/0929867323666160122115057 |
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