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Chen. Neuroimmunol Neuroinflammation 2016;3:268-70 Neuroimmunology and
DOI: 10.20517/2347-8659.2016.46
Neuroinflammation

www.nnjournal.net
Editorial Open Access

Endocannabinoid metabolism in

neurodegenerative diseases

Chu Chen

Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA 70112, USA.
Correspondence to: Dr. Chu Chen, Neuroscience Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center,
2020 Gravier Street, New Orleans, LA 70112, USA. E-mail: cchen@lsuhsc.edu; chen502@gmail.com
How to cite this article: Chen C. Endocannabinoid metabolism in neurodegenerative diseases. Neuroimmunol Neuroinflammation 2016;3:268-70.
Article history: Received: 14-11-2016 Accepted: 15-11-2016 Published: 15-12-2016

Dr. Chu Chen is a tenured professor in the Neuroscience Center of Excellence, Louisiana State University
Health Sciences Center in New Orleans, USA. The research programs in Dr. Chen’s laboratory focus on
neuroinflammation in health and disease. His current research interests are in endocannabinoid signaling in
neurodegenerative diseases.

Endocannabinoids are endogenous lipid mediators inflammatory and neuroprotective properties. [4,5]
contributing to a variety of physiological,
pharmacological, and pathological processes primarily 2-AG is synthesized largely from diacylglycerol by
through acting on cannabinoid receptors (CB1R and diacylglycerol lipase α and β and primarily hydrolyzed
CB2R), which are targets of Δ -tetrahydrocannabinol by the enzyme monoacylglycerol lipase (MAGL)
9
(Δ -THC), the major psychoactive ingredient to glycerol and arachidonic acid (AA), a precursor
9
in marijuana. [1] Although N-arachidonoyl of prostaglandins and leukotrienes [Figure 1]. And
ethanolamide is the first identified endocannabinoid, 2-AG is also degraded by the enzymes α/β hydrolase
2-arachidonoylglycerol (2-AG), the second identified domain-containing protein 6 and 12 and metabolized
endocannabinoid, is the most abundant ligand oxidatively by cyclooxygenase 2 (COX-2). Apparently,
produced in our body and a full agonist for CB1R 2-AG is a very unstable bioactive lipid mediator, and it is
and CB2R. It has been well recognized that 2-AG easily and rapidly degraded by these enzymes upon its
[2]
[2]
is a retrograde messenger modulating synaptic synthesis. It has been estimated that 85% of 2-AG is
transmission and plasticity at both inhibitory metabolized by MAGL in the brain. Arachidonic acid-
[6]
GABAergic and excitatory glutamatergic synapses delivered prostaglandins and leukotrienes are generally
in the brain. [2-4] In particular, augmentation of 2-AG proinflammatory and neurotoxic, whereas 2-AG is
signaling by inhibition of its metabolism has been capable of resolving neuroinflammation and protecting
attracted attention recently due to its profound anti- neurons from harmful insults. [4,5,7] This suggests that

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