An international team of researchers at by Universities of Bristol and Exeter and published in Nature Communications, has identified a gene in the brain that drives anxiety symptoms. Modification of the gene is shown to reduce anxiety levels, offering an exciting new drug target for anxiety disorders.
Anxiety disorders are common with 1 in 4 people diagnosed with a disorder at least once in their lifetime. Severe psychological trauma can trigger changes in neurons in the brain’s amygdala, leading to the onset of anxiety disorders.
However, the efficacy of currently available anti-anxiety drugs is low with more than half of patients not achieving remission following treatment. In this study, scientists sought to identify the molecular events in the brain that underpin anxiety. They focused on a group of molecules known as miRNAs, which regulate multiple target proteins controlling the cellular processes in the amygdala.
Following acute stress, the team found an increased amount of one type of molecule called miR483-5p in a mouse amygdala. Importantly, the team showed that increased miR483-5p suppressed the expression of another gene, Pgap2, which in turn drives changes to neuronal morphology in the brain and behaviour associated with anxiety. Together, the researchers showed that miR-483-5p acts as a molecular brake that offsets stress-induced amygdala changes to promote anxiety relief.
The discovery of this novel pathway through which the brain regulates its response to stress offers potential for the development of anti-anxiety therapies for complex psychiatric conditions in humans.
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