Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress

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 inflam...

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Main Authors: Julie E. Finnell, Susan K. Wood
Format: Article
Language:English
Published: Elsevier 2016-10-01
Series:Neurobiology of Stress
Online Access:http://www.sciencedirect.com/science/article/pii/S235228951530045X
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spelling doaj-89c927b1c86a42f2b63a63a4982d9af02020-11-24T22:34:56ZengElsevierNeurobiology of Stress2352-28952016-10-014C11410.1016/j.ynstr.2016.04.001Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stressJulie E. FinnellSusan K. WoodA 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.http://www.sciencedirect.com/science/article/pii/S235228951530045X
collection DOAJ
language English
format Article
sources DOAJ
author Julie E. Finnell
Susan K. Wood
spellingShingle Julie E. Finnell
Susan K. Wood
Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress
Neurobiology of Stress
author_facet Julie E. Finnell
Susan K. Wood
author_sort Julie E. Finnell
title Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress
title_short Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress
title_full Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress
title_fullStr Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress
title_full_unstemmed Neuroinflammation at the interface of depression and cardiovascular disease: Evidence from rodent models of social stress
title_sort neuroinflammation at the interface of depression and cardiovascular disease: evidence from rodent models of social stress
publisher Elsevier
series Neurobiology of Stress
issn 2352-2895
publishDate 2016-10-01
description 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.
url http://www.sciencedirect.com/science/article/pii/S235228951530045X
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