Why Does Fear Persist? Deciphering the Brain’s New World | GeneOnline News

Researchers at Linköping University in Sweden have discovered a biological mechanism that can increase the strength of fear memory in the brain. Research on mice, published in the journal Molecular Psychiatry, publishes new insights into the mechanisms behind anxiety and identificationsanxietyand common mechanisms underlying alcohol addiction.

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What is fear?

For humans, the ability to feel fear is essential to escape 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 the inability of the affected patient. Researchers suspect that some people are more prone to morbid fear tendencies, caused by a disturbance in the way the brain processes frightening memories. Certain areas of the brain are particularly important for processing fear-related memories. When a threat is experienced, the amygdala activates and works with the frontal lobe, the prefrontal cortex, which regulates emotions.

Molecular mechanisms involved in fear

For a long time, humans have done thismolecularThe mechanism is still unknown. The researchers studied 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 addiction and leads to excessive stress response. It is common for both alcohol addiction and anxiety-related disorders to coexist in humans, so the researchers suspected this was due to a common mechanism behind these disorders and studied the effect of PRDM2 reduction on fear memory processing. The researchers identified the genes that were affected when the PRDM2 index was reduced and it was clear that these genes would lead to increased activity in the nerve cells that connect 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 a down-regulation of PRDM2, but there is still no way to increase its concentration. Thus, this mechanism may be part of explaining why some people are more prone to anxiety-related disorders and why these disorders and alcohol addiction coexist so frequently, and this biological mechanistic discovery can provide insights into one direction. for future research and development of fear control drugs.

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