Poster Presentations

Abstract

Background : Recently, a tentative model of Stress-Induced Depression (STR-I-D) was proposed. The aetiology and development of STRI-D is suggested to be mediated by four neurobiological mechanisms: monoamine dysfunction, hypothalamo-pituitary adrenocortical axis dysfunction, neurogenesis dysfunction and neuroinfl ammation. While exercise is an effective adjunct or standalone therapy in the treatment and prevention of depressive disorders, its neurobiological basis is poorly understood and warrants further investigation. Objectives : To review the literature on the neurobiological mechanisms involved in the aetiology and development of STR-I-D and to review the infl uence of exercise on these neurobiological mechanisms and how it may be useful to prevent or attenuate STR-I-D. Methods : The author systematically reviewed the scientific literature on the subject over the last 30 years, searching PubMed, OvidSP and ScienceDirect databases. Main search terms included: neurotrophin, neuroinflammation, monoamine, hypothesis, psychological stress, murine, human and translational. Findings : Chronic psychological stress has a multitude of effects on the central nervous system which are known to contribute to the development of depression. These include a reduction in serotonin levels, hypercortisolaemia, reduced brain-derived neurotrophic factor and elevated proinfl ammatory cytokines (i.e. tumour necrosis factor alpha and interleukin-6). Findings are consistent across murine-based models and human studies. Preliminary data suggests exercise has beneficial effects on these same neurobiological processes, which take part in the development of depression. Conclusions : Current literature suggests an association between the four neurobiological mechanisms, STR-I-D and exercise. Further research into these mechanisms is needed to improve diagnostic recognition, predict treatment response and to provide a basis for efficient, individualised therapies.