New Study Discovered The Mechanism That Causes Fear Memories To Get “Stuck” In Our Brains

Drobot Dean - illustrative purpose only, not the actual person
Drobot Dean - illustrative purpose only, not the actual person

Fear is a natural and critical part of the “fight or flight” response that helps humans escape and avoid threatening situations.

But, while fear is a key factor of ensuring survival, the emotion can also become excessive.

For example, people with anxiety-related disorders or post-traumatic stress disorder (PTSD) often experience persistent and excessive fear reactions even while in safe situations. This can result in ongoing anxiety and a severely decreased quality of life.

But, researchers from Linkoping University in Sweden suspected that these pathological fears are caused by a disruption in how the brain processes fearful memories.

“We know that the network of nerve cells that connect the frontal lobes to the amygdala is involved in fear responses. And the connections between these brain structures are altered in people with PTSD and other anxiety disorders,” explained Estelle Barbier, the study’s lead author.

However, the exact molecular mechanisms involved have not been identified until now.

The researchers conducted a study on rats and identified PRDM2– a protein that actually suppresses gene expression.

And interestingly, PRDM2 levels are typically lower in instances of alcohol dependence and lead to more significant stress responses.

Additionally, it is common for anxiety-related conditions and alcohol dependence to coexist– which led the researchers to believe that there are common mechanisms behind both conditions.

Drobot Dean – illustrative purpose only, not the actual person

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More specifically, the team analyzed how low levels of PRDM2 impact the way memories are processed and stored– a process known as “consolidation.” And they found that down-regulation of PRDM2 actually increases the storage of fearful memories.

Unfortunately, though, researchers do not currently have a way of increasing PRDM2 to weaken or erase fear memories. Nonetheless, Barbier still believes this finding is groundbreaking in further illuminating chronic fear response processes.

“The mechanism may be part of the explanation of why some individuals have a greater vulnerability to developing anxiety-related conditions. It may also explain why these conditions and alcohol dependence so often are present together,” she said.

Still, further research regarding if and how PRDM2 levels might be manipulated to lessen fear responses is warranted.

To read the study’s complete findings, which have since been published in Molecular Psychiatry, visit the link here.

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