This study looks at conditions such as Post-Traumatic Stress Disorder (PTSD) as well as other conditions stemming from fear, stress, and anxiety, through the targeting of Fatty Acid Amide Hydrolase (FAAH) to increase the efficiency of Anandamide’s (AEA) interactions with the ECS and different areas of the brain as a potential treatment for PTSD. Preclinical research shows that ECS activity influences functional connectivity between the prefrontal cortex and amygdala and thereby influences an organism’s ability to cope with threats and stressful experiences. Animal studies show that CB1 receptor activation within the amygdala is essential for extinction of fear memories. Failure to extinguish traumatic memories is a core symptom of PTSD, suggesting that potentiating ECS signalling may have a therapeutic potential in this condition.
This premise was to find potential alternative ways of targeting the ECS, as past medications (most notably rimonabant) that have been made available have been pulled due to adverse side-effects.
Analysis shows that, in contrast to other areas of neuropsychopharmacology, effects of endocannabinoid modulation on the regulation of fear and stress responses have so far translated from preclinical studies to humans. These effects are particularly encouraging in the context of PTSD treatment, as they target the core pathophysiological mechanisms of extinction-resistant fear and exaggerated stress responses, rather than merely mitigating symptoms.
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