A Randomized Controlled Trial of the Tumor Necrosis Factor Antagonist Infliximab for Treatment-Resistant Depression

Raison, Charles L.; Rutherford, Robin E.; Woolwine, Bobbi J.; Chen, Shuo; Schettler, Pamela J.; Drake, Daniel; Haroon, Ebrahim; Miller, Andrew H.

doi:10.1001/2013.jamapsychiatry.4

Cited by 1,355 publications

(1,151 citation statements)

References 74 publications

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“…However, distinguishing this 'inflammatory subtype' of depression from other non-inflammatory subtypes has been more challenging, and currently there are no behavioral or neural phenotypic data for understanding the basis of these differences, which is necessary for precision-based intervention development (although C-reactive protein (CRP) levels have been used as a physiological biomarker for this difference; Raison et al, 2013).…”

Section: Differentiating Inflammatory-mediated Depression From Other mentioning

confidence: 99%

In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior

Eisenberger

Moieni

Inagaki

et al. 2016

Neuropsychopharmacol

291

220

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Although it has commonly been assumed that the immune system and the processes that govern social behavior are separate, non-communicating entities, research over the past several decades suggests otherwise. Considerable evidence now shows that inflammatory processes and social behavior are actually powerful regulators of one another. This review first summarizes evidence that inflammatory processes regulate social behavior, leading to characteristic changes that may help an individual navigate the social environment during times of sickness. Specifically, this review shows that inflammation: (1) increases threatrelated neural sensitivity to negative social experiences (eg, rejection, negative social feedback), presumably to enhance sensitivity to threats to well-being or safety in order to avoid them and (2) enhances reward-related neural sensitivity to positive social experiences (eg, viewing close others and receiving positive social feedback), presumably to increase approach-related motivation towards others who might provide support and care during sickness. Next, this review summarizes evidence showing that social behavior also regulates aspects of inflammatory activity, preparing the body for situations in which wounding and infection may be more likely (social isolation). Here, we review research showing: (1) that exposure to social stressors increases proinflammatory activity, (2) that individuals who are more socially isolated (ie, lonely) show increased proinflammatory activity, and (3) that individuals who are more socially isolated show increased proinflammatory activity in response to an inflammatory challenge or social stressor. The implications of the co-regulation of inflammation and social behavior are discussed.

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Section: Differentiating Inflammatory-mediated Depression From Other mentioning

confidence: 99%

In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior

Eisenberger

Moieni

Inagaki

et al. 2016

Neuropsychopharmacol

291

220

View full text Add to dashboard Cite

show abstract

“…And in experimental models, SSRIs attenuate lipopolysaccharide-induced inflammation [91]. A variety of more traditional antiinflammatory therapies has also been used for the treatment of depression, including aspirin and other nonsteroidal antiinflammatory drugs, statins, and cytokine inhibitors like etanercept (which blocks TNF) [92][93][94][95]. Agomelatine is a a b c d member of a novel class of new antidepressants which are melatonin agonists; it has been approved by the European Union, after being shown to have similar efficacy to SSRIs for the treatment of depression [96,97].…”

Section: Therapeutic Approaches To the Treatment Of Depression: A Focmentioning

confidence: 99%

Inflammation and the Silent Sequelae of Stroke

Becker

2016

Neurotherapeutics

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Depression and fatigue are common after stroke and negatively impact the quality of life of stroke survivors. The biological bases of these symptoms are unknown, but an abundance of data point to a role for inflammation. This review highlights evidence supporting the contribution of inflammation to poststroke depression and poststroke fatigue. Potential treatments for poststroke depression and poststroke fatigue are explored, with a special emphasis on those that modulate the immune response.

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“…Moreover, gene expression profiling conducted on post-mortem brain tissue samples from the frontal cortex of patients with MDD shows an upregulated expression of cytokines including eg IL-1, IL-18, IL-8, IL-12, lymphotoxin alpha and interferon (IFN)- (Shelton et al, 2011). More direct evidence for the involvement of cytokines in the pathophysiology of MDD comes from the observations that (i) anti-TNF treatment has therapeutic effects in resistant MDD with increased CRP (Raison et al, 2013), and (ii) the development of depressed mood, anxious symptoms and impaired cognition in human patients treated with type I interferons ( (Miller et al, 2009)). Likewise, in mice, the systemic or intracerebroventricular administration of cytokines or cytokine inducers leads to depressive-like behavior (Fu et al, 2010).…”

mentioning

confidence: 99%

Depression in Autoimmune Diseases

Pryce

Fontana

2016

Current Topics in Behavioral Neurosciences

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Up to 50% of patients with autoimmune diseases show an impairment of health-related quality of life and exhibit depression-like symptoms. The immune system not only leads to inflammation in affected organs, but also mediates behavior abnormalities including fatigue and depression-like symptoms. This review focuses on the different pathways involved in the communication of the immune system with the neuronal network and the body's timing system. The latter is built up by a hierarchically organized expression of clock genes. As discussed here, the activation of the immune system interferes with high amplitude expression of clock genes, an effect which may play a pivotal role in depression-like behavior in autoimmune diseases.

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A Randomized Controlled Trial of the Tumor Necrosis Factor Antagonist Infliximab for Treatment-Resistant Depression

Cited by 1,355 publications

References 74 publications

In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior

In Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior

Inflammation and the Silent Sequelae of Stroke

Depression in Autoimmune Diseases

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