Scientists have discovered differences in the mechanisms of memory of experienced fear in men and women

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A team of scientists from Virginia Tech has discovered a molecular mechanism in the brains of female rats associated with the formation and storage of memories of traumatic events. This feature was not found in males. In the future, the discovery could help create more effective treatments for post-traumatic stress disorder (PTSD) and Alzheimer's disease, taking into account the patient's biological sex. The study results were published in the journal Behavioral Brain Research.

It is known that women experience PTSD approximately twice as often as men. Scientists speculate that this may be due to differences in the way male and female brains process and store memories of fear. One of the possible mechanisms causing the difference may be a previously poorly studied molecular process—K27 polyubiquitination.

“Women suffer from PTSD more often than men, but they do not report experiencing more traumatic events. This suggests the existence of a neurobiological mechanism that is activated in women during traumatic experiences and may help explain differences in the prevalence of PTSD between the sexes,” said study leader Timothy Jarome.

In an experiment with rats, the researchers targeted two areas of the brain associated with fear and memory: the hippocampus, which helps associate events with specific places and circumstances, and the amygdala, which is responsible for processing emotions.

After experiencing a frightening experience, female rats showed an increase in K27 polyubiquitination in the hippocampus; no such changes were recorded in males. At the same time, conditioned fear reflexes did not cause significant reactions in the amygdala in either males or females.

“We would expect to see similar activity in the amygdala, since this region plays a key role in emotional reactions. However, we found it in a broader memory system, and exclusively in one sex,” Jarome emphasized.

To confirm the result, scientists artificially reduced K27 levels using genetic engineering techniques. As a result, females lost memories of the fear they experienced, while such interventions had no noticeable effect on males.

“Just because males and females are equally capable of learning and remembering events does not mean that their brains use the same mechanisms to do so. If we are developing treatments for conditions such as PTSD or looking for ways to improve memory, we may need different approaches for men and women,” Jarome said.

The researchers also found that during memory formation in females, biomacr K27 attaches to a specific protein, ACAT1. This protein has been linked to the development of Alzheimer's disease, which affects the hippocampus and leads to memory impairment. New research suggests that ACAT1 may be involved in both long-term memory formation and memory loss.

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