期刊
NEUROIMMUNOMODULATION
卷 17, 期 3, 页码 192-195出版社
KARGER
DOI: 10.1159/000258721
关键词
Post-traumatic stress disorder; Cortisol; Hypocortisolism; Cytokines; Inflammation; Lymphocytes
Early life stress has been suggested to mediate vulnerability to affective disorders. Traumatic events experienced in childhood such as sexual abuse and/or physical neglect may lead to psychiatric diseases in adult life, including post-traumatic stress disorder ( PTSD). Previous studies have focused on adult traumatic events and very little is known regarding the long-term physiological effects of early life stress. Here, we review the complex interplay between most important cognitive, neuroendocrine and immunological changes reported in PTSD, focusing on long-term implications of childhood maltreatment. PTSD has been associated with significant biological changes related to impaired cognitive functions, attenuated hypothalamic-pituitary-adrenal (HPA) axis function (hypocortisolism) and activation of innate immune responses (low-grade inflammation). Copyright (C) 2010 S. Karger AG, Basel
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