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Adenosine A1 and A2A Receptors in the Brain: Current Research and Their Role in Neurodegeneration
The inhibitory adenosine A1 receptor (A1R) and excitatory A2A receptor (A2AR) are predominantly expressed in the brain. Whereas the A2AR has been implicated in normal aging and enhancing neurotoxicity in multiple neurodegenerative diseases, the inhibitory A1R has traditionally been ascribed to have...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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MDPI
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6154612/ https://www.ncbi.nlm.nih.gov/pubmed/28441750 http://dx.doi.org/10.3390/molecules22040676 |
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author | Stockwell, Jocelyn Jakova, Elisabet Cayabyab, Francisco S. |
author_facet | Stockwell, Jocelyn Jakova, Elisabet Cayabyab, Francisco S. |
author_sort | Stockwell, Jocelyn |
collection | PubMed |
description | The inhibitory adenosine A1 receptor (A1R) and excitatory A2A receptor (A2AR) are predominantly expressed in the brain. Whereas the A2AR has been implicated in normal aging and enhancing neurotoxicity in multiple neurodegenerative diseases, the inhibitory A1R has traditionally been ascribed to have a neuroprotective function in various brain insults. This review provides a summary of the emerging role of prolonged A1R signaling and its potential cross-talk with A2AR in the cellular basis for increased neurotoxicity in neurodegenerative disorders. This A1R signaling enhances A2AR-mediated neurodegeneration, and provides a platform for future development of neuroprotective agents in stroke, Parkinson’s disease and epilepsy. |
format | Online Article Text |
id | pubmed-6154612 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-61546122018-11-13 Adenosine A1 and A2A Receptors in the Brain: Current Research and Their Role in Neurodegeneration Stockwell, Jocelyn Jakova, Elisabet Cayabyab, Francisco S. Molecules Review The inhibitory adenosine A1 receptor (A1R) and excitatory A2A receptor (A2AR) are predominantly expressed in the brain. Whereas the A2AR has been implicated in normal aging and enhancing neurotoxicity in multiple neurodegenerative diseases, the inhibitory A1R has traditionally been ascribed to have a neuroprotective function in various brain insults. This review provides a summary of the emerging role of prolonged A1R signaling and its potential cross-talk with A2AR in the cellular basis for increased neurotoxicity in neurodegenerative disorders. This A1R signaling enhances A2AR-mediated neurodegeneration, and provides a platform for future development of neuroprotective agents in stroke, Parkinson’s disease and epilepsy. MDPI 2017-04-23 /pmc/articles/PMC6154612/ /pubmed/28441750 http://dx.doi.org/10.3390/molecules22040676 Text en © 2017 by the authors. 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 (http://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Review Stockwell, Jocelyn Jakova, Elisabet Cayabyab, Francisco S. Adenosine A1 and A2A Receptors in the Brain: Current Research and Their Role in Neurodegeneration |
title | Adenosine A1 and A2A Receptors in the Brain: Current Research and Their Role in Neurodegeneration |
title_full | Adenosine A1 and A2A Receptors in the Brain: Current Research and Their Role in Neurodegeneration |
title_fullStr | Adenosine A1 and A2A Receptors in the Brain: Current Research and Their Role in Neurodegeneration |
title_full_unstemmed | Adenosine A1 and A2A Receptors in the Brain: Current Research and Their Role in Neurodegeneration |
title_short | Adenosine A1 and A2A Receptors in the Brain: Current Research and Their Role in Neurodegeneration |
title_sort | adenosine a1 and a2a receptors in the brain: current research and their role in neurodegeneration |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6154612/ https://www.ncbi.nlm.nih.gov/pubmed/28441750 http://dx.doi.org/10.3390/molecules22040676 |
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