The role of inflammation in core features of depression: Insights from paradigms using exogenously-induced inflammation.

Neurosci Biobehav Rev

Cousins Center for Psychoneuroimmunology, Semel Institute for Neuroscience & Human Behavior, University of California Los Angeles, Los Angeles, CA 90095, USA; Department of Psychology, University of California Los Angeles, Los Angeles, CA 90095, USA.

Published: November 2018


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Article 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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6192535PMC
http://dx.doi.org/10.1016/j.neubiorev.2018.09.006DOI Listing

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