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A group of German, Israeli and British scientists have found that a gene-based approach offers promise for development of a treatment for highly stressful experiences and PTSD. The team discovered that extreme stress induces a change in the expression of the acetylcholinesterase gene. Under normal circumstances, this gene produces a vital protein that adheres to neuronal synapses. Following stress, however, the same gene produces large quantities of a protein with modified properties that results in heightened electrical signals in the nerve cells communicating through these synapses. This results in reactions of extreme fright or immobilizing shock.
According to an article in Molecular Psychiatry, the scientists have succeeded in developing an "antisense" agent that acts to neutralize the process whereby a modified protein is produced, thus preventing the "extreme" reaction associated with traumatic memory-inducing stimuli. If the stressful memory is later reignited via an object, a sound, an image or other form of association, that same neuronal reaction can happen. With this new approach, the reactions are suppressed but not the memory itself. The researchers believe that since the memory of dangerous situations or circumstances can be beneficial for survival, their goal is to develop a drug that would block the harmful reactions of those suffering from recurring stress symptoms due to lingering memories of past traumatic experiences. Until now there has been no drug to treat the core of the post-stress problem, but rather only its symptoms.
Previous studies by some of the same researchers show an evolution in this line of thinking about cholinergic gene expression and stress reactions. The hope of this team is to create a commercial medicinal product based on this line of research.
Structural roles of acetylcholinesterase variants in biology and pathology
Acute stress facilitates long-lasting changes in cholinergic gene expression
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