, 2012). Thus, there is an imperative need for effective treatments for childhood PTSD. This review highlights one of the few examples where research in animals has helped lead to treatments
for human brain disorders. Since the PFC expands greatly in evolution, work in nonhuman primates has been particularly important for revealing the molecular mechanisms to protect and normalize PFC physiology in humans. Continued research is needed to help develop treatments that alleviate the suffering of patients exposed to trauma. AFTA is supported by an NIH Director’s Pioneer Award DP1AG047744-01. The research described in this review has been funded by a wide variety of sources. Disclosures: AFTA and Yale University receive royalties from Shire Pharmaceuticals from the sales of Intuniv™ (extended release find more guanfacine) for the treatment of pediatric selleck chemicals llc ADHD. “
“The acute stress response, characterized by activation of the sympathetic nervous system, the hypothalamus-pituitary-adrenal axis and the
immune system, is a physiologically adaptive response that enables the organism to deal with environmental threats. However, when the stress exposure is chronic, prolonged activation of the stress response may become maladaptive and have adverse consequences for the individual. In addition to disorders directly linked to stress exposure, like post traumatic stress disorder, risk of the development of Thymidine kinase several other disorders such as affective disorders, type 2 diabetes and cardiovascular disease have been associated with stress (reviewed in (de Kloet et al., 2005)). Chronic stress during adulthood may have adverse consequences, but the effects of stress exposure during gestation or early childhood may have more severe consequences as it may alter brain development and thereby have long-term consequences on adult phenotype. The idea that the early life environment may alter adult phenotype is described in the Developmental Origins of Health and Disease (DOHaD) hypothesis. This hypothesis states that adverse conditions during the early life period may result in persistent changes in physiology and metabolism that in
turn alter risk for disease development in adulthood and was first proposed by David Modulators Barker (Barker, 1988). Therefore, this hypothesis was initially referred to as the “Barker Hypothesis”. This hypothesis was based on the observation that low birth weight was associated with increased risk for coronary heart disease in adulthood (Barker and Osmond, 1986). Over the last decades more data supporting this hypothesis have become available from studies in both humans as well as in animal models. Evidence that this hypothesis may hold true comes from epidemiological studies in individuals who were exposed to adverse environmental conditions, like natural disasters or war, showing increased risk for metabolic, immune and stress-related disorders later in life.