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New study from the University of Florida Department of Neuroscience finds anti-inflammatory agents do not yield beneficial effects in treating addiction disorders.
Methamphetamine (METH), a psychostimulant subject to abuse worldwide, is widely recognized for its effects on dopamine neurotransmission and the central nervous system (CNS). In recent years, questions of METH’s effects on microglial neuroimmune functions, neuroinflammation, and dopaminergic neurotoxicity have been investigated. Microglia are resident immune cells of the CNS responsible for a wide range of neuroimmune functionality including brain development, maintenance of neural networks through removal of dead or damaged cells, and injury repair. The chronic activation of these microglial cells can lead to long-term neural damage.
The current review reports microglial activation after METH administration in rodents gives a fair assessment of the nature and severity of METH toxicity. Conclusions from these studies note microglial activation as “quite modest,” indicating minimal damage to the dopaminergic neurons.
This led UF neuroscientists’ conclusion to stand in contrast to the belief that neuroinflammation contributes to and intensifies METH neurotoxicity.
This research can be beneficial in understanding and treating addiction disorders in the future.