For the first time, British researchers have identified a genetic pathway in the brain that plays a key role in controlling anxiety, opening the door to the development of more effective treatments in the future.
One in four people will be diagnosed with an anxiety disorder at least once in their lifetime, and it usually presents as recurring episodes of intense anxiety, dread, or sudden feelings of dread that peak within minutes.
Severe psychological trauma is known to trigger genetic, biochemical and structural changes in a part of the brain called the amygdala, a complex structure located in the temporal lobe. This is the area that processes fear and threatening stimuli, and has been linked to stress-induced anxiety, which can lead to anxiety disorders, including panic attacks and post-traumatic stress disorder (PTSD).
Current anti-anxiety medications are not particularly effective, and more than half of people do not achieve remission after treatment. Researchers from the Universities of Bristol and Exeter believe that the ineffectiveness of these drugs is due to a lack of understanding of the brain circuits and molecular interactions that lead to anxiety.
“Stress triggers the onset of many neuropsychiatric disorders rooted in an unfavorable combination of genetic and environmental factors,” said Valentina Mosienko, corresponding author of the study. “While low levels of stress are counteracted by the brain’s natural ability to adjust, severe or prolonged traumatic experiences can overcome the protective mechanisms of stress recovery, leading to the development of pathological conditions such as depression or anxiety.”
The research team decided to investigate these molecular causes of anxiety, focusing on microRNAs (miRNAs), small non-coding RNA segments that coordinate complex brain responses by regulating target genes.
The researchers tested mice and found that acute stress increased a specific miRNA, miR-483-5p, in the mouse amygdala.Then miR-483-5p represses the function of this gene P gap 2, It is responsible for altering neurons in the amygdala and driving anxiety-related behaviors.
In short, researchers find that miR-483-5p acts as a “molecular brake” Gap 2 gene, reduces stress-induced changes in the amygdala, thereby reducing anxiety.
This is the first discovery of miR-483-5p/Gap 2 path. A better understanding of the mechanisms that underpin anxiety provided by research could lead to the development of more effective treatments for this often debilitating condition.
“miRNAs are strategically poised to control complex neuropsychiatric disorders such as anxiety,” Mosienko said. “But the molecular and cellular mechanisms they use to regulate stress resilience and susceptibility have been largely unknown until now. miR-483-5p/Gap 2 The pathways we identified in this study, the activation of which produces an anxiety-reducing effect, offer great potential for the development of anxiolytic treatments for complex psychiatric disorders in humans. “
The study was published in the journal natural communication.
source: University of Bristol