Endocannabinoid metabolism and traumatic brain injury

Research output: Contribution to journalReview articlepeer-review

7 Scopus citations

Abstract

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.

Original languageEnglish (US)
Article number2979
JournalCells
Volume10
Issue number11
DOIs
StatePublished - Nov 2021

Keywords

  • Alzheimer’s disease
  • Cannabinoid receptor
  • Endocannabinoid
  • Monoacylglycerol lipase
  • Proliferator-activated receptor γ
  • Traumatic brain injury

ASJC Scopus subject areas

  • General Biochemistry, Genetics and Molecular Biology

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