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Brain Inflammation Secondary To TBI Can Be Limited

Benjamin Cravatt, Ph.D., at the Scripps Research Institute and Daniel Nomura, Ph.D., at UC Berkeley have made an important discovery about how to block brain inflammation, something which can severely compound the initial damage done by a TBI. They learned that in the brain the production of arachidonic acid (which gets converted into the pro-inflammatory substances called prostaglandins) is controlled chiefly by the enzyme MAGL(monoacylglycerol lipase). MAGL uses the enzyme 2-AG to make arachidonic acid. 2-AG is a cannabinoid associated with pain reduction and pleasure production which mimics the effects of marijuana.

The research scientists showed that by blocking the activity of MAGL they could shrink of the pool of arachidonic acid and prostaglandins in mouse brains and effectively limit the amount of brain inflammation in mice. Brain inflammation (which occurs in Alzheimer’s and Parkinson’s diseases) is also a major problem following TBI, and limiting brain inflammation following TBI would prevent secondary damage. The researchers will continue studying the most effective ways to eliminate MAGL from the brain or to block its actions.