The neurobiological background of posttraumatic stress symptomatology throughout the lifespan

Altered neurobiological functioning of neural, physiological and endocrine systems are associated with posttraumatic stress disorder (PTSD). It has become increasingly clear that the developmental timing of adversity and neurobiological functioning influence the risk to develop PTSD and other stress-related and comorbid disorders throughout life. Yet, the exact involved neural, endocrine and cardiac mechanisms are still largely unknown and hampers us to improve our understanding of who is at risk for PTSD symptom development. In this dissertation, it was investigated how timing of adversity during different periods across the lifespan (prenatal, early life, adulthood) impacts the development of PTSD symptomatology and the vulnerability of stress-related neurobiological processes. The chapters of this thesis demonstrated time-dependent effects of adversity, with mostly but not always the same structures and systems involved in PTSD symptom development in adolescents and adults. Adversity might thus affect the regulation and functioning of these structures and systems differently depending on the timing of exposure. This work also highlighted that interindividual differences in vulnerabilities in these neurobiological stress processes, genetic factors and sex appeared to explain variation in PTSD risk and symptom outcome, with accumulation of adverse events throughout life including early neurodevelopmental periods considered to be an important influencing factor. This knowledge may contribute to the understanding of varied PTSD risk and improved future interventions that may help people to grow and flourish despite adversity.