| Literature DB >> 30201219 |
Larissa N Dooley1, Kate R Kuhlman2, Theodore F Robles3, Naomi I Eisenberger3, Michelle G Craske4, Julienne E Bower3.
Abstract
A wealth of evidence has implicated inflammation in the development of depression. Yet, the heterogeneous nature of depression has impeded efforts to understand, prevent, and treat the disease. The purpose of this integrative review is to summarize the connections between inflammation and established core features of depression that exhibit more homogeneity than the syndrome itself: exaggerated reactivity to negative information, altered reward processing, decreased cognitive control, and somatic syndrome. For each core feature, we first provide a brief overview of its relevance to depression and neurobiological underpinnings, and then review evidence investigating a potential role of inflammation. We focus primarily on findings from experimental paradigms of exogenously-induced inflammation. We conclude that inflammation likely plays a role in exaggerated reactivity to negative information, altered reward reactivity, and somatic symptoms. There is less evidence supporting an effect of inflammation on cognitive control as assessed by standard neuropsychological measures. Finally, we discuss implications for future research and recommendationsfor how to test the role of inflammation in the pathogenesis of heterogeneous psychiatric disorders.Entities:
Keywords: Cognitive control; Depression; Endophenotype; Inflammation; Mood; Reward; Somatic
Mesh:
Year: 2018 PMID: 30201219 PMCID: PMC6192535 DOI: 10.1016/j.neubiorev.2018.09.006
Source DB: PubMed Journal: Neurosci Biobehav Rev ISSN: 0149-7634 Impact factor: 8.989