Key result
Stress-induced neuroinflammation may serve as a key mechanism underlying the high rate of comorbidity between psychosocial disorders like depression and cardiovascular disease.
Stress-induced neuroinflammation may be a key mechanistic link between depression and cardiovascular disease.
Neuroinflammation may link depression and CVD; leaves open whether targeting it improves outcomes in comorbid patients.
A large body of evidence has emerged linking stressful experiences, particularly from one's social environment, with psychiatric disorders. However, vast individual differences emerge in susceptibility to developing stress-related pathology which may be due to distinct differences in the inflammatory response to social stress. Furthermore, depression is an independent risk factor for cardiovascular disease, another inflammatory-related disease, and results in increased mortality in depressed patients. This review is focused on discussing evidence for stress exposure resulting in persistent or sensitized inflammation in one individual while this response is lacking in others. Particular focus will be directed towards reviewing the literature underlying the impact that neuroinflammation has on neurotransmitters and neuropeptides that could be involved in the pathogenesis of comorbid depression and cardiovascular disease. Finally, the theme throughout the review will be to explore the notion that stress-induced inflammation is a key player in the high rate of comorbidity between psychosocial disorders and cardiovascular disease.
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Finnell et al. (2016) conducted a review in Depression and cardiovascular disease. Social stress was evaluated. Stress-induced neuroinflammation may serve as a key mechanism underlying the high rate of comorbidity between psychosocial disorders like depression and cardiovascular disease.
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