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Scientists may have found something, though
.
A new study from UT Health San Antonio, published Feb.
"Previous research by my lab and others has found that pharmacological inhibition of MAGL reduces neuropathology in traumatic brain injury and improves cognitive function," said senior author Chu Chen, Ph.
D.
, professor of cellular and integrative physiology at UT Health San Antonio
.
However, the mechanism is unclear and cannot explain why disrupting the enzyme has so many beneficial effects
On both counts, the answer is yes
.
The researchers found:
Whole brain (or total) knockdown of MAGL produced neuroprotective effects similar to drug inhibition
.Knockout of MAGL in astrocytes significantly reduced brain injury disease effects and cognitive decline in TBI animals
.On the other hand, knocking out MAGL in neurons did not protect animals from tbi-induced disease
.
Neurons are message messengers in the brain and spinal cord
.
Nerve impulses are passed from one neuron to another throughout the body
In the brain, 2-AG is mainly synthesized by neurons, and there is also a small amount of 2-AG in astrocytes
.
"However, even a small amount of 2-AG in astrocytes could have a dramatic effect on tbi-induced neuronal damage, which was completely beyond our original expectations," said Dr.
"The most exciting thing our study revealed is that 2-AG metabolism in astrocytes, but not neurons, promotes neuropathology, and that MAGL inactivation in astrocytes increases 2-AG signaling, plays an important role in neuroprotection from tbi-induced injury," said Dr.
Collectively, these findings point to the need to develop therapeutic interventions that inhibit astrocytic 2-AG degradation, he said
Journal Reference :
Mei Hu, Dexiao Zhu, Jian Zhang, Fei Gao, Jack Hashem, Philip Kingsley, Lawrence J Marnett, Ken Mackie, Chu Chen.
