TY - JOUR
T1 - The Bidirectional Relationship of Depression and Inflammation
T2 - Double Trouble
AU - Beurel, Eléonore
AU - Toups, Marisa
AU - Nemeroff, Charles B.
N1 - Funding Information:
Work in the author’s labs is supported by the NIH ( MH104656 , MH110415 , MH117293 , MH115326 , AA024933 ).
Funding Information:
Work in the author's labs is supported by the NIH (MH104656, MH110415, MH117293, MH115326, AA024933). C.B.N.?s financial disclosures are as follows: consulting for the last three years for Xhale, Takeda, Taisho Pharmaceutical Inc. Signant Health, Sunovion Pharmaceuticals Inc. Janssen Research & Development LLC, Magstim, Inc. Navitor Pharmaceuticals, Inc. Sunovion, TC MSO, Inc. Intra-Cellular Therapies, Inc. EMA Wellness, Gerson Lehrman Group (GLG), and Acadia Pharmaceuticals; a stockholder in Xhale, Celgene, Seattle Genetics, Abbvie, OPKO Health, Inc. Antares, BI Gen Holdings, Inc. Corcept Therapeutics Pharmaceuticals Company, TC MSO, Inc. Trends in Pharma Development, LLC, and EMA Wellness; on the scientific advisory boards of the American Foundation for Suicide Prevention (AFSP), Brain and Behavior Research Foundation (BBRF), Xhale, Anxiety Disorders Association of America (ADAA), Skyland Trail, Signant Health, Laureate Institute for Brain Research (LIBR), Inc.; and a member of the Board of Directors of AFSP, Gratitude America, ADAA, and Xhale Smart, Inc. C.B.N. also reports income sources or equity of $10,000 or more in American Psychiatric Publishing, Xhale, Signant Health, CME Outfitters, Intra-Cellular Therapies, Inc. Magstim, and EMA Wellness; patents for method and devices for transdermal delivery of lithium (US 6,375,990B1); method of assessing antidepressant drug therapy via transport inhibition of monoamine neurotransmitters by ex vivo assay (US 7,148,027B2); and compounds, compositions, methods of synthesis, and methods of treatment (CRF Receptor Binding Ligand) (US 8,551, 996 B2).
PY - 2020/7/22
Y1 - 2020/7/22
N2 - Depression represents the number one cause of disability worldwide and is often fatal. Inflammatory processes have been implicated in the pathophysiology of depression. It is now well established that dysregulation of both the innate and adaptive immune systems occur in depressed patients and hinder favorable prognosis, including antidepressant responses. In this review, we describe how the immune system regulates mood and the potential causes of the dysregulated inflammatory responses in depressed patients. However, the proportion of never-treated major depressive disorder (MDD) patients who exhibit inflammation remains to be clarified, as the heterogeneity in inflammation findings may stem in part from examining MDD patients with varied interventions. Inflammation is likely a critical disease modifier, promoting susceptibility to depression. Controlling inflammation might provide an overall therapeutic benefit, regardless of whether it is secondary to early life trauma, a more acute stress response, microbiome alterations, a genetic diathesis, or a combination of these and other factors.
AB - Depression represents the number one cause of disability worldwide and is often fatal. Inflammatory processes have been implicated in the pathophysiology of depression. It is now well established that dysregulation of both the innate and adaptive immune systems occur in depressed patients and hinder favorable prognosis, including antidepressant responses. In this review, we describe how the immune system regulates mood and the potential causes of the dysregulated inflammatory responses in depressed patients. However, the proportion of never-treated major depressive disorder (MDD) patients who exhibit inflammation remains to be clarified, as the heterogeneity in inflammation findings may stem in part from examining MDD patients with varied interventions. Inflammation is likely a critical disease modifier, promoting susceptibility to depression. Controlling inflammation might provide an overall therapeutic benefit, regardless of whether it is secondary to early life trauma, a more acute stress response, microbiome alterations, a genetic diathesis, or a combination of these and other factors.
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U2 - 10.1016/j.neuron.2020.06.002
DO - 10.1016/j.neuron.2020.06.002
M3 - Review article
C2 - 32553197
AN - SCOPUS:85088041392
VL - 107
SP - 234
EP - 256
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 2
ER -