Endocannabinoid Metabolism and Traumatic Brain Injury

Traumatic brain injury (TBI) represents a major cause of morbidity and disability and is a risk factor for developing neurodegenerative diseases, including Alzheimer’s disease (AD). However, no effective therapies are currently available for TBI-induced AD-like disease. Endocannabinoids are endogeno...

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Autores principales:	Dexiao Zhu, Fei Gao, Chu Chen
Formato:	article
Lenguaje:	EN
Publicado:	MDPI AG 2021
Materias:	endocannabinoid cannabinoid receptor traumatic brain injury Alzheimer’s disease monoacylglycerol lipase proliferator-activated receptor γ Biology (General) QH301-705.5
Acceso en línea:	https://doaj.org/article/9d698df39bc24a438ac5670d93fe8bef
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spelling	oai:doaj.org-article:9d698df39bc24a438ac5670d93fe8bef2021-11-25T17:09:59ZEndocannabinoid Metabolism and Traumatic Brain Injury10.3390/cells101129792073-4409https://doaj.org/article/9d698df39bc24a438ac5670d93fe8bef2021-11-01T00:00:00Zhttps://www.mdpi.com/2073-4409/10/11/2979https://doaj.org/toc/2073-4409Traumatic brain injury (TBI) represents a major cause of morbidity and disability and is a risk factor for developing neurodegenerative diseases, including Alzheimer’s disease (AD). However, no effective therapies are currently available for TBI-induced AD-like disease. Endocannabinoids are endogenous lipid mediators involved in a variety of physiological and pathological processes. The compound 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid with profound anti-inflammatory and neuroprotective properties. This molecule is predominantly metabolized by monoacylglycerol lipase (MAGL), a key enzyme degrading about 85% of 2-AG in the brain. Studies using animal models of inflammation, AD, and TBI provide evidence that inactivation of MAGL, which augments 2-AG signaling and reduces its metabolites, exerts neuroprotective effects, suggesting that MAGL is a promising therapeutic target for neurodegenerative diseases. In this short review, we provide an overview of the inhibition of 2-AG metabolism for the alleviation of neuropathology and the improvement of synaptic and cognitive functions after TBI.Dexiao ZhuFei GaoChu ChenMDPI AGarticleendocannabinoidcannabinoid receptortraumatic brain injuryAlzheimer’s diseasemonoacylglycerol lipaseproliferator-activated receptor γBiology (General)QH301-705.5ENCells, Vol 10, Iss 2979, p 2979 (2021)
institution	DOAJ
collection	DOAJ
language	EN
topic	endocannabinoid cannabinoid receptor traumatic brain injury Alzheimer’s disease monoacylglycerol lipase proliferator-activated receptor γ Biology (General) QH301-705.5
spellingShingle	endocannabinoid cannabinoid receptor traumatic brain injury Alzheimer’s disease monoacylglycerol lipase proliferator-activated receptor γ Biology (General) QH301-705.5 Dexiao Zhu Fei Gao Chu Chen Endocannabinoid Metabolism and Traumatic Brain Injury
description	Traumatic brain injury (TBI) represents a major cause of morbidity and disability and is a risk factor for developing neurodegenerative diseases, including Alzheimer’s disease (AD). However, no effective therapies are currently available for TBI-induced AD-like disease. Endocannabinoids are endogenous lipid mediators involved in a variety of physiological and pathological processes. The compound 2-arachidonoylglycerol (2-AG) is the most abundant endocannabinoid with profound anti-inflammatory and neuroprotective properties. This molecule is predominantly metabolized by monoacylglycerol lipase (MAGL), a key enzyme degrading about 85% of 2-AG in the brain. Studies using animal models of inflammation, AD, and TBI provide evidence that inactivation of MAGL, which augments 2-AG signaling and reduces its metabolites, exerts neuroprotective effects, suggesting that MAGL is a promising therapeutic target for neurodegenerative diseases. In this short review, we provide an overview of the inhibition of 2-AG metabolism for the alleviation of neuropathology and the improvement of synaptic and cognitive functions after TBI.
format	article
author	Dexiao Zhu Fei Gao Chu Chen
author_facet	Dexiao Zhu Fei Gao Chu Chen
author_sort	Dexiao Zhu
title	Endocannabinoid Metabolism and Traumatic Brain Injury
title_short	Endocannabinoid Metabolism and Traumatic Brain Injury
title_full	Endocannabinoid Metabolism and Traumatic Brain Injury
title_fullStr	Endocannabinoid Metabolism and Traumatic Brain Injury
title_full_unstemmed	Endocannabinoid Metabolism and Traumatic Brain Injury
title_sort	endocannabinoid metabolism and traumatic brain injury
publisher	MDPI AG
publishDate	2021
url	https://doaj.org/article/9d698df39bc24a438ac5670d93fe8bef
work_keys_str_mv	AT dexiaozhu endocannabinoidmetabolismandtraumaticbraininjury AT feigao endocannabinoidmetabolismandtraumaticbraininjury AT chuchen endocannabinoidmetabolismandtraumaticbraininjury
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Endocannabinoid Metabolism and Traumatic Brain Injury

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