Gene Triggering Anxiety Symptoms Identified

Anxiety triggering gene identified
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An international team of scientists has uncovered a gene in the brain that is responsible for anxious feelings. Importantly, gene alteration has been found to lessen anxiety levels, providing an attractive new therapeutic target for anxiety disorders. The discovery, conducted by academics from the Universities of Bristol and Exeter, was published in Nature Communications today (April 25). Anxiety disorders are common, with one out of every four people being diagnosed with one at some point in their lives. Severe psychological trauma can cause genetic, physiological, and morphological alterations in neurons in the amygdala of the brain—the brain region implicated in stress-induced anxiety—resulting in the formation of anxiety disorders such as panic attacks and post-traumatic stress disorder.

However, the efficacy of currently available anti-anxiety medications is poor, with more than half of patients failing to achieve remission after treatment. Our limited success in generating effective anxiolytic (anti-anxiety) medications is due to our lack of understanding of the brain circuits underpinning anxiety and the molecular mechanisms that occur in stress-related neuropsychiatric disorders. The goal of this study was to uncover the chemical events in the brain that underpin anxiety. In animal models, they concentrated on a class of chemicals called as miRNAs. This crucial collection of molecules, which is also found in the human brain, regulates several target proteins that control cellular processes in the amygdala.

Following acute stress, the researchers discovered an increase in the number of one type of molecule known as miR483-5p in the mouse amygdala. Importantly, the researchers discovered that elevated miR483-5p expression reduced the expression of another gene, Pgap2, which in turn causes alterations in neuronal architecture in the brain and anxiety-related behavior. The researchers discovered that miR-483-5p functions as a molecular brake, offsetting stress-induced amygdala alterations and promoting anxiety alleviation.

The discovery of a unique amygdala miR483-5p/Pgap2 pathway by which the brain modulates its response to stress is the first step toward the development of novel, more potent, and much-needed medicines for anxiety disorders that will improve this pathway.

“Stress can trigger the onset of a number of neuropsychiatric conditions that have their roots in an adverse combination of genetic and environmental factors,” said Dr. Valentina Mosienko, one of the study’s lead authors and an MRC Fellow and Lecturer in Neuroscience at Bristol’s School of Physiology, Pharmacology, and Neuroscience. While mild levels of stress are balanced by the brain’s inherent ability to adapt, severe or protracted traumatic experiences can overwhelm the protective mechanisms of stress resilience, leading to the development of pathological diseases.

“miRNAs are strategically poised to control complex neuropsychiatric conditions. But the molecular and cellular mechanisms they use to regulate stress resilience and susceptibility were until now, largely unknown. The miR483-5p/Pgap2 pathway we identified in this study, activation of which exerts anxiety-reducing effects, offers a huge potential for the development of anti-anxiety therapies for complex psychiatric conditions in humans.”

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