by A recent study conducted by researchers from the Central Institute of Mental Health (CIMH) and Heidelberg University has identified a biological mechanism that influences the strength of memories related to aversive events. This breakthrough research provides new insights that could pave the way for the development of innovative therapies for psychiatric disorders.
Fear memories are essential for an organism’s survival as they facilitate appropriate responses to environmental stimuli. However, traumatic experiences can result in the formation of intense fear memories, which are linked to mental health conditions like post-traumatic stress disorder (PTSD).
The team of scientists from CIMH and Heidelberg University uncovered a biological process that may contribute to regulating resilience to adverse life events. Their findings, published in the journal Molecular Psychiatry, shed light on a potential mechanism that could impact the strength of aversive memories.
In cases of PTSD, individuals often exhibit exaggerated fear responses unrelated to the original trauma. Current therapies, such as exposure therapy focused on fear memory extinction, have limitations in effectively addressing these symptoms. Dr. Ana M. M. Oliveira and her research group at CIMH delved into biological mechanisms that could potentially prevent the formation of intense fear memories.
Through experiments involving mice, the researchers observed that experiencing a traumatic event triggered two distinct phases of heightened Npas4 protein levels in the mouse brain, whereas a less severe event only induced one phase. Interestingly, the second phase of Npas4 seemed to act as a safeguard against the development of overpowering fear memories.
By blocking the second phase of Npas4, the researchers noticed a stronger fear memory that was resistant to extinction, leading to exaggerated fear responses. Conversely, inducing the second phase of Npas4 resulted in a decrease in fear memory strength, accompanied by reduced fear reactions in unrelated situations.
Npas4, a protein crucial for neuronal communication, was found to play a key role in regulating fear memory formation. The researchers demonstrated that the dual increase in Npas4 protein levels after a traumatic event led to higher levels of the neurotransmitter GABA, which suppresses neuronal activity. This mechanism may explain how Npas4 influences fear memory control.
Dr. Ana M. M. Oliveira highlighted the importance of future research to uncover why this protective mechanism can sometimes fail, allowing pathological memories to emerge. Ultimately, this study has unveiled a potential molecular target that could be leveraged for the development of novel therapies targeting psychiatric disorders.
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1. Source: Coherent Market Insights, Public sources, Desk research
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