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Microglial Endocannabinoid Signalling in AD

Chronic inflammation in Alzheimer’s disease (AD) has been recently identified as a major contributor to disease pathogenesis. Once activated, microglial cells, which are brain-resident immune cells, exert several key actions, including phagocytosis, chemotaxis, and the release of pro- or anti-inflam...

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Autores principales: Scipioni, Lucia, Ciaramellano, Francesca, Carnicelli, Veronica, Leuti, Alessandro, Lizzi, Anna Rita, De Dominicis, Noemi, Oddi, Sergio, Maccarrone, Mauro
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8997504/
https://www.ncbi.nlm.nih.gov/pubmed/35406803
http://dx.doi.org/10.3390/cells11071237
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author Scipioni, Lucia
Ciaramellano, Francesca
Carnicelli, Veronica
Leuti, Alessandro
Lizzi, Anna Rita
De Dominicis, Noemi
Oddi, Sergio
Maccarrone, Mauro
author_facet Scipioni, Lucia
Ciaramellano, Francesca
Carnicelli, Veronica
Leuti, Alessandro
Lizzi, Anna Rita
De Dominicis, Noemi
Oddi, Sergio
Maccarrone, Mauro
author_sort Scipioni, Lucia
collection PubMed
description Chronic inflammation in Alzheimer’s disease (AD) has been recently identified as a major contributor to disease pathogenesis. Once activated, microglial cells, which are brain-resident immune cells, exert several key actions, including phagocytosis, chemotaxis, and the release of pro- or anti-inflammatory mediators, which could have opposite effects on brain homeostasis, depending on the stage of disease and the particular phenotype of microglial cells. The endocannabinoids (eCBs) are pleiotropic bioactive lipids increasingly recognized for their essential roles in regulating microglial activity both under normal and AD-driven pathological conditions. Here, we review the current literature regarding the involvement of this signalling system in modulating microglial phenotypes and activity in the context of homeostasis and AD-related neurodegeneration.
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spelling pubmed-89975042022-04-12 Microglial Endocannabinoid Signalling in AD Scipioni, Lucia Ciaramellano, Francesca Carnicelli, Veronica Leuti, Alessandro Lizzi, Anna Rita De Dominicis, Noemi Oddi, Sergio Maccarrone, Mauro Cells Review Chronic inflammation in Alzheimer’s disease (AD) has been recently identified as a major contributor to disease pathogenesis. Once activated, microglial cells, which are brain-resident immune cells, exert several key actions, including phagocytosis, chemotaxis, and the release of pro- or anti-inflammatory mediators, which could have opposite effects on brain homeostasis, depending on the stage of disease and the particular phenotype of microglial cells. The endocannabinoids (eCBs) are pleiotropic bioactive lipids increasingly recognized for their essential roles in regulating microglial activity both under normal and AD-driven pathological conditions. Here, we review the current literature regarding the involvement of this signalling system in modulating microglial phenotypes and activity in the context of homeostasis and AD-related neurodegeneration. MDPI 2022-04-06 /pmc/articles/PMC8997504/ /pubmed/35406803 http://dx.doi.org/10.3390/cells11071237 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
Scipioni, Lucia
Ciaramellano, Francesca
Carnicelli, Veronica
Leuti, Alessandro
Lizzi, Anna Rita
De Dominicis, Noemi
Oddi, Sergio
Maccarrone, Mauro
Microglial Endocannabinoid Signalling in AD
title Microglial Endocannabinoid Signalling in AD
title_full Microglial Endocannabinoid Signalling in AD
title_fullStr Microglial Endocannabinoid Signalling in AD
title_full_unstemmed Microglial Endocannabinoid Signalling in AD
title_short Microglial Endocannabinoid Signalling in AD
title_sort microglial endocannabinoid signalling in ad
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8997504/
https://www.ncbi.nlm.nih.gov/pubmed/35406803
http://dx.doi.org/10.3390/cells11071237
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