Study discovers ‘anxiety gene’ and how to disable it – 06/20/2023 – Equilibrium

Scientists have identified a mechanism in the amygdala associated with anxiety disorder, paving the way for possible development of new drugs to treat serious conditions. About a quarter of people experience an anxiety disorder at some point in their lives, which can be accompanied by panic attacks and PTSD (post-traumatic stress disorder).

In some cases, intense and prolonged psychological trauma can cause genetic, biochemical and morphological changes in neurons in the amygdala, a region of the brain that acts in the control of emotional reactions, such as anxiety.

The effectiveness of drugs currently available to control the disorder, however, is low, and more than half of patients fail to get rid of symptoms with treatment. One of the reasons for this low effectiveness is the poor understanding of how neurons and molecular events act to trigger anxiety.

A study conducted by researchers from the British universities of Bristol and Exeter and published in the scientific journal Nature Communications brought clues that may contribute to the development of more effective remedies.

The research managed to identify a gene that, when suppressed, leads to reduced anxiety.

How the study was done

The researchers subjected laboratory rats to 6 h of stress and then extracted their cerebral tonsils and analyzed them.

Five microRNAs, molecules involved in activating genes and converting them into proteins, were found to be in higher than normal concentrations in these animals subjected to stress. The same group of molecules is found in the human brain.

Of these microRNAs, the one that was in greater quantity in the tonsils was miR-483-5p. After a series of tests, the researchers discovered that the miR-483-5p was related to a specific gene that acts in anxiety episodes, the Pgap2.

The research found that when miR-483-5p levels were higher, expression of the Pgap2 gene was inhibited, which in turn reduced anxiety levels. According to the study, miR-483-5p works as a “molecular brake” that reduces amygdala activity that promotes anxiety.

practical applications

Valentina Mosiensko, a professor at the University of Bristol and one of the authors of the study, says that stress can trigger the emergence of several neuropsychiatric conditions caused by an adverse combination of genetic and environmental factors.

“Although low levels of stress are counterbalanced by the brain’s natural ability to adjust, severe or prolonged traumatic experiences can overwhelm the protective mechanisms of stress resilience, leading to the development of pathological conditions such as depression or anxiety,” he said.

She points out that microRNAs are positioned to control complex neuropsychiatric conditions such as anxiety, but their mechanisms of action are still poorly understood.

“The miR483-5p/Pgap2 pathway we identified in this study, whose activation exerts anxiety-reducing effects, offers enormous potential for the development of anti-anxiety therapies for complex psychiatric conditions in humans,” he said.