How memories of fear get stuck in some minds

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“How memories of fear get stuck in some minds”

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Researchers at Linköping University in Sweden have discovered a biological mechanism that increases the strength with which fear memories are stored in the brain. The study conducted on mice was published in the scientific journal Molecular Psychiatry. It provides new knowledge about the mechanisms underlying anxiety-related disorders, and identifies the common mechanisms behind anxiety and alcohol dependence.

The ability to feel fear is essential to escaping life-threatening situations and learning how to avoid them in the future. However, in some cases, such as post-traumatic stress disorder (PTSD) and other anxiety-related disorders, fear reactions become excessive, persisting even when they are not appropriate. This raises serious concern even though the danger is no longer present, and disables the affected person. Researchers believe that some individuals have a greater tendency to develop pathological fears, and that this is caused by disturbances in the way the brain processes fearful memories.

Certain areas of the brain are especially important for processing fear-related memories. The amygdala is activated when exposed to threats, and works in conjunction with parts of the brain’s frontal lobes, the ‘frontal cortex’, which are important for regulating emotions.

“We know that the network of neurons connecting the frontal lobes to the amygdala is involved in fear responses. The connections between these brain structures are altered in people with PTSD and other anxiety disorders,” says Estelle Barbier, associate professor at the Center for Neuroscience. Social and Affective Sciences (CSAN), and the Department of Biomedical and Clinical Sciences (BKV) at Linköping University who led the study.

However, the molecular mechanisms involved remained unknown for a long time. In the current study, the researchers investigated a protein known as PRDM2, an epigenetic enzyme that suppresses the expression of several genes. Researchers have previously found that PRDM2 levels are lower in alcohol dependence, and lead to excessive stress responses. In people, it is very common for alcoholism and anxiety-related conditions to co-exist, and researchers suspect that this is due to the common mechanisms behind these conditions.

For new memories to last, they must be etched and preserved as long-term memories. This process is known as “consolidation”. In the current study, researchers investigated the effects of low PRDM2 levels on the way fear memories are processed.

“We have identified a mechanism in which increased activity in the network between the frontal lobe and the amygdala increases acquired fear responses. We have shown that negative regulation of PRDM2 increases the consolidation of fear-related memories,” says Estelle Barbier.

The researchers also identified genes that are affected when the level of PRDM2 is low. This turned out to be an increase in the activity of neurons connecting the frontal lobe and the amygdala.

Patients with anxiety disorders may benefit from treatments that weaken or erase fear memories. The biological mechanism we have identified involves down-regulation of PRDM2, and we currently have no way to increase it. But the mechanism may be part of the explanation for why some individuals are more prone to developing anxiety-related conditions. It may also explain why these conditions and alcohol dependence often exist together,” says Estelle Barbier.

Reference: Ricardo B, Canat C, Michel B, et al. An epigenetic mechanism of excessive consolidation of fear memories. Psychiatry Mall. 2022 doi: 10.1038 / s41380-022-01758-6

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