An international team of scientists, led by researchers from the Universities of Bristol and Exeter, has identified a gene in the brain that drives anxiety symptoms. The discovery could be a promising drug target for anxiety disorders, as modifying the gene has been shown to reduce anxiety levels.
Anxiety disorders affect one in four people during their lifetime, and they can be triggered by severe psychological trauma, leading to genetic, biochemical, and morphological changes in neurons in the brain’s amygdala – the region associated with stress-induced anxiety.
Current anti-anxiety drugs have limited efficacy, with over half of patients not achieving remission after treatment. This is due to our incomplete understanding of the neural circuits and molecular events related to anxiety and stress-related neuropsychiatric conditions.
The scientists focused on a group of molecules called miRNAs in animal models, which also exist in the human brain and regulate various target proteins that control cellular processes in the amygdala. After acute stress, they found an increased amount of a specific molecule called miR483-5p in the mouse amygdala. This molecule suppressed the expression of another gene, Pgap2, which is responsible for changes in neuronal morphology in the brain and anxiety-related behaviors.
The researchers discovered that miR-483-5p acts as a molecular brake, offsetting stress-induced changes in the amygdala and promoting anxiety relief.
This novel discovery of the amygdala miR483-5p/Pgap2 pathway offers a potential path to develop more potent and much-needed treatments for anxiety disorders. Understanding and enhancing this pathway could pave the way for new anti-anxiety therapies to address complex psychiatric conditions in humans.
Dr. Valentina Mosienko, one of the study’s lead authors, stated that miRNAs play a critical role in controlling complex neuropsychiatric conditions like anxiety, and the identified pathway offers great potential for the development of effective anti-anxiety therapies for such conditions.