A deeper view into the effects of repetitive traumatic stress on aging

Abstract

An attack, or even the perception of a predator elicits a rapid “fight-or-flight” response to enhance the animal’s chance of survival. In mammals, the acute fight-or-flight response leads to the release of catecholamines (CA). Perpetuated activation of this acute stress response, as is the case of patients suffering from post-traumatic stress disorder (PTSD) is associated with accelerated aging. Nevertheless the molecular and cellular mechanisms that underlie this detrimental effect remain largely obscure. Taking advantage of its relative simple anatomy, genetics, high degree of conservation and short lifespan, we introduced a model of the nematode C. elegans, to go deep into these mechanisms. C. elegans coordinates stress response by releasing the CA tyramine (TA), the structural and functional counterpart of adrenaline in mammals. We here determined that TA-deficient animals (tdc-1) exhibit increased healthspan and lifespan. On contrary, animals permanently exposed to acute stressors, have reduced lifespan and deteriorated general fitness. These detrimental effects are not observed in tdc-1 mutants suggesting that they depend on TA release. We are currently performing experiments in order to explore how neuronal architecture and function are affected by persistent activation of the fear-related response. This study was aimed to unravel how the stress response impacts on the structural, cellular and functional changes that normally occur with aging.