Why does fear linger? Deciphering the new world of the brain | GeneOnline News

Researchers at Linköping University in Sweden have discovered a biological mechanism that may increase the strength of fear memory storage in the brain.The research in mice, published in the journal Molecular Psychiatry, publishes new knowledge regarding the mechanisms behind anxiety and identifiesanxietyand common mechanisms behind alcohol dependence.

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What is fear?

For humans, the ability to experience fear is essential to escape from life-threatening situations and learn how to avoid them in the future. However, in some cases, such as post-traumatic stress disorder (PTSD) and other anxiety-related disorders, fear can become an overreaction and persist even in situations where it is no longer appropriate to express anxiety. Even if the danger is no longer present, this can trigger intense anxiety and lead to incapacitation of the affected patient. The researchers suspect that some people are more prone to morbid fearful tendencies, caused by a disturbance in the way the brain processes fearful memories. Certain areas of the brain are particularly important for processing fear-related memories. When a threat is experienced, the amygdala is activated and works with the frontal lobe, the prefrontal cortex, that regulates emotion.

Molecular mechanisms involved in fear

For a long time, humans havemolecularThe mechanism is still unknown. The researchers investigated a protein called PRDM2, an epigenetic enzyme that inhibits the expression of many genes. It has now been found that the PRDM2 index is lower in people with alcohol dependence and leads to an excessive stress response. It is common for both alcohol dependence and anxiety-related disorders to coexist in humans, so the researchers suspected that this was due to a common mechanism behind these disorders, and investigated the effect of reduced PRDM2 on fear memory processing. The researchers identified genes that were affected when the PRDM2 index was reduced, and it was clear that these genes would lead to increased activity in nerve cells connecting the frontal lobe to the amygdala.

Therefore, researchers believe that patients suffering from anxiety disorders can be improved by treatments that weaken or eliminate fear memory. The biological mechanism that has been identified so far involves down-regulation of PRDM2, but there is still no way to increase its concentration. Thus, this mechanism may be part of the explanation for why some people are more prone to anxiety-related disorders, and why these disorders and alcohol dependence coexist so frequently, and this biological mechanistic discovery may provide insights into A direction for future research and development of fear control drugs.

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References:

https://www.eurekalert.org/news-releases/965076

https://www.nature.com/articles/s41380-022-01758-6

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