Glial Modulation by N-acylethanolamides in Brain Injury and Neurodegeneration

Neuroinflammation involves the activation of glial cells and represents a key element in normal aging and pathophysiology of brain damage. N-acylethanolamides (NAEs), naturally occurring amides, are known for their pro-homeostatic effects. An increase in NAEs has been reported in vivo and in vitro i...

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Autores principales: Herrera, María I., Kölliker-Frers, Rodolfo, Barreto, George, Blanco, Eduardo, Capani, Francisco
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2016
Materias:
Neuroscience
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844606/
https://www.ncbi.nlm.nih.gov/pubmed/27199733
http://dx.doi.org/10.3389/fnagi.2016.00081
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author Herrera, María I.
Kölliker-Frers, Rodolfo
Barreto, George
Blanco, Eduardo
Capani, Francisco
author_facet Herrera, María I.
Kölliker-Frers, Rodolfo
Barreto, George
Blanco, Eduardo
Capani, Francisco
author_sort Herrera, María I.
collection PubMed
description Neuroinflammation involves the activation of glial cells and represents a key element in normal aging and pathophysiology of brain damage. N-acylethanolamides (NAEs), naturally occurring amides, are known for their pro-homeostatic effects. An increase in NAEs has been reported in vivo and in vitro in the aging brain and in brain injury. Treatment with NAEs may promote neuroprotection and exert anti-inflammatory actions via PPARα activation and/or by counteracting gliosis. This review aims to provide an overview of endogenous and exogenous properties of NAEs in neuroinflammation and to discuss their interaction with glial cells.
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spelling pubmed-48446062016-05-19 Glial Modulation by N-acylethanolamides in Brain Injury and Neurodegeneration Herrera, María I. Kölliker-Frers, Rodolfo Barreto, George Blanco, Eduardo Capani, Francisco Front Aging Neurosci Neuroscience Neuroinflammation involves the activation of glial cells and represents a key element in normal aging and pathophysiology of brain damage. N-acylethanolamides (NAEs), naturally occurring amides, are known for their pro-homeostatic effects. An increase in NAEs has been reported in vivo and in vitro in the aging brain and in brain injury. Treatment with NAEs may promote neuroprotection and exert anti-inflammatory actions via PPARα activation and/or by counteracting gliosis. This review aims to provide an overview of endogenous and exogenous properties of NAEs in neuroinflammation and to discuss their interaction with glial cells. Frontiers Media S.A. 2016-04-26 /pmc/articles/PMC4844606/ /pubmed/27199733 http://dx.doi.org/10.3389/fnagi.2016.00081 Text en Copyright © 2016 Herrera, Kölliker-Frers, Barreto, Blanco and Capani. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Neuroscience
Herrera, María I.
Kölliker-Frers, Rodolfo
Barreto, George
Blanco, Eduardo
Capani, Francisco
Glial Modulation by N-acylethanolamides in Brain Injury and Neurodegeneration
title Glial Modulation by N-acylethanolamides in Brain Injury and Neurodegeneration
title_full Glial Modulation by N-acylethanolamides in Brain Injury and Neurodegeneration
title_fullStr Glial Modulation by N-acylethanolamides in Brain Injury and Neurodegeneration
title_full_unstemmed Glial Modulation by N-acylethanolamides in Brain Injury and Neurodegeneration
title_short Glial Modulation by N-acylethanolamides in Brain Injury and Neurodegeneration
title_sort glial modulation by n-acylethanolamides in brain injury and neurodegeneration
topic Neuroscience
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4844606/
https://www.ncbi.nlm.nih.gov/pubmed/27199733
http://dx.doi.org/10.3389/fnagi.2016.00081
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