Discovery of a revolutionary method to “turn off” anxiety

Researchers are struggling to find effective drugs for anxiety. However, controlling the expression of certain genes could be the answer, according to a new study that shows promising results in mice.

A novel target to fight anxiety

A team of scientists from the Universities of Bristol and Exeter has discovered a new target for the development of anti-anxiety drugs. The approach is based on stimulating a series of genes whose expression naturally reduces anxiety.

Finding new treatments is crucial as anxiety cases continue to rise worldwide. According to the World Organization, by 2019, more than 300 million people had been diagnosed with an anxiety disorder, including 58 million and adolescents. The situation worsened after the COVID-19 pandemic, with an increase in anxiety and depression cases.

Limited access to psychologists and ineffectiveness of current medications

Unfortunately, access to psychologists remains difficult. For example, in Spain, there are few psychologists in the public health system for the number of people affected, and not everyone can afford a private psychologist. This is the first problem to be solved. In the meantime, many people turn to anti-anxiety medications, often recommended by their doctors. However, these treatments are not effective enough. In many cases, the desired effect is not achieved, mainly because the neural mechanisms at the origin of anxiety are not well understood. This is why the researchers' discovery is so important.

Anti-anxiety drugs based on gene expression

To understand the function of different genes, scientists turn them on and off to observe the resulting effects. This can be done through a variety of methods, including the use of miRNAs – molecules that regulate gene expression.

In this study, the researchers used the miRNA miR483-5p, which acts in the amygdala, a region of the brain involved in the regulation of emotions, and thus linked to anxiety. By manipulating this miRNA in the brain of mice, they found that miR483-5p acts on the Pgap2 gene, which in turn causes changes in neuronal morphology and behavior associated with anxiety. Thus, this miRNA is able to block the effects of stress induced in the amygdala, inhibiting anxiety.

If this occurs naturally, why do we have anxiety?

One might ask why some people suffer from anxiety if this natural mechanism exists. The answer lies in the fact that it only works at reduced stress levels.

Everyone experiences moments of stress, but if they are occasional, we do not develop an anxiety disorder. This is due, among other reasons, to regulators like this one. However, when the stress is caused by an acute traumatic event or persists for a long time, the natural mechanisms are no longer sufficient.

This is where therapy and, in some cases, anti-anxiety medications come in. Thus, if a drug could further increase the effect of this miRNA, it might be possible to curb anxiety even in the presence of greater stress.

This discovery opens the door to new anti-anxiety drugs. In the meantime, and even afterwards, we must not forget that psychological therapy is essential. It is therefore necessary to continue to fight so that all people can have access to it, regardless of their financial resources.

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