Inflammation and clinical response to treatment in depression: A meta-analysis

Strawbridge, Rebecca; Arnone, Danilo; Danese, Andrea; Papadopoulos, Andrew; Herane-Vives, Andrés; Cleare, Anthony J.

doi:10.1016/j.euroneuro.2015.06.007

Cited by 546 publications

(412 citation statements)

References 67 publications

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“…Of note, IDO inhibitors are actively being developed as anticancer agents, and are therefore currently available for testing (Lob et al, 2009). Because inhibition of serotonin transporters and increasing serotonin availability is a primary mechanism of action of conventional antidepressants, the capacity of inflammatory cytokines to increase serotonin transporter expression and function, while also reducing serotonin synthesis, may serve to undermine the ability of SSRIs to treat mood and anxiety disorders, consistent with the observation that inflammation is associated with treatment nonresponse Strawbridge et al, 2015).…”

Section: Inflammation Effects On Neurotransmitter Metabolismmentioning

confidence: 73%

“…The impact of epigenetic changes in FKBP5 are in part related to the induction of glucocorticoid resistance and reduced hormonal (glucocorticoid) control of inflammatory responses as reflected by decreased sensitivity to the synthetic glucocorticoid dexamethasone in vitro following LPS stimulation (Klengel et al, 2013). Relative to treatment response, it should also be noted that increased inflammatory markers have been associated with treatment nonresponse, such that patients with evidence of increased inflammation before antidepressant treatment exhibit reduced treatment responsiveness, and patients who are defined as treatment resistant exhibit increased inflammatory markers (Sluzewska et al, 1997;Lanquillon et al, 2000;Raison et al, 2013a, b;Strawbridge et al, 2015).…”

Section: Foundations For the Hypothesis That The Immune System Playsmentioning

confidence: 99%

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Therapeutic Implications of Brain–Immune Interactions: Treatment in Translation

Miller

Haroon

Felger

2016

Neuropsychopharmacol

118

124

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A wealth of data has been amassed that details a complex, yet accessible, series of pathways by which the immune system, notably inflammation, can influence the brain and behavior. These data have opened the window to a diverse array of novel targets whose potential efficacy is tied to specific neurotransmitters and neurocircuits as well as specific behaviors. What is clear is that the impact of inflammation on the brain cuts across psychiatric disorders and engages dopaminergic and glutamatergic pathways that regulate motivation and motor activity as well as the sensitivity to threat. Given the ability to identify patient populations with increased inflammation, the precision of interventions can be further tuned, in conjunction with the ability to establish target engagement in the brain through the use of multiple neuroimaging strategies. After a brief overview of the mechanisms by which inflammation affects the brain and behavior, this review examines the extant literature on the efficacy of anti-inflammatory treatments, while forging guidelines for future intelligent clinical trial design. An examination of the most promising therapeutic strategies is also provided, along with some of the most exciting clinical trials that are currently being planned or underway.

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Section: Inflammation Effects On Neurotransmitter Metabolismmentioning

confidence: 73%

Section: Foundations For the Hypothesis That The Immune System Playsmentioning

confidence: 99%

Therapeutic Implications of Brain–Immune Interactions: Treatment in Translation

Miller

Haroon

Felger

2016

Neuropsychopharmacol

118

124

View full text Add to dashboard Cite

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“…Additionally, the lack of healthy controls hampered the interpretation of the results. Circulating TNFα levels are affected by various metabolic and pathological conditions in addition to MDD (McArdle, Finucane, Connaughton, McMorrow, & Roche, 2013; Sinha et al, 2015). Moreover, plasma TNFα levels may be affected by anesthesia during ECT series (Stelzhammer et al., 2011).…”

Section: Discussionmentioning

confidence: 99%

Low tumor necrosis factor‐α levels predict symptom reduction during electroconvulsive therapy in major depressive disorder

et al. 2018

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ObjectiveChanges in the tumor necrosis factor‐α (TNFα) have been associated with major depressive disorder (MDD). Findings concerning the effects of electroconvulsive therapy (ECT) on the TNFα level have been contradictory. The aim was to examine the immediate and long‐term changes in the TNFα level and their associations with symptom reduction in patients with MDD during ECT.MethodThe study included 30 patients with MDD. Their TNFα levels were measured at baseline and 2 and 4 hr after the first, fifth and last ECT session. Depressive symptoms were assessed with the Montgomery‐Asberg Depression Rating Scale (MADRS).ResultsThe TNFα level decreased from baseline to the 2‐ and 4‐hr measurements. There was a correlation between the first ECT session TNFα levels and the relative symptom reduction according to the MADRS score after the ECT series. Both the first (baseline) ECT and 4‐hr TNFα levels were lower in responders than in nonresponders.Conclusion ECT consistently induced a decrease in the TNFα level after each studied session. A low TNFα level at the first ECT appeared to predict a symptom reduction. These findings suggest that TNFα might have a role in the pathogenesis in MDD and in the mechanism of action of ECT.

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“…Longitudinal studies found that the elevated inflammation levels observed in depressed individuals likely result from bidirectional associations between depression and inflammation over time (Matthews et al, 2010). Of note, elevation in inflammation levels is more obvious in depressed patients with recurrent course of illness (Ford and Erlinger, 2004) and those who are resistant to conventional treatment strategies (Strawbridge et al, 2015).…”

Section: Observational Studies In Humansmentioning

confidence: 99%

“…Furthermore, both childhood trauma (Varese et al, 2012;Widom, 1999;Widom et al, 2007) and early-life immune activation (see Inflammation and Psychopathology: Observational Human Studies) are associated with a large range of psychiatric disorders, including depression, bipolar disorder, schizophrenia, and PTSD. Finally, both factors appear to be associated not only with higher risk of incident disorders, but also with unfavorable longitudinal course of illness and treatment response (Agnew-Blais and Danese, 2016;Berk et al, 2011;Ford and Erlinger, 2004;Nanni et al, 2012;Strawbridge et al, 2015).…”

Section: Analogymentioning

confidence: 99%

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

Danese

Lewis

2016

Neuropsychopharmacol

305

191

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The brain and the immune system are not fully formed at birth, but rather continue to mature in response to the postnatal environment. The two-way interaction between the brain and the immune system makes it possible for childhood psychosocial stressors to affect immune system development, which in turn can affect brain development and its long-term functioning. Drawing from experimental animal models and observational human studies, we propose that the psychoneuroimmunology of early-life stress can offer an innovative framework to understand and treat psychopathology linked to childhood trauma. Earlylife stress predicts later inflammation, and there are striking analogies between the neurobiological correlates of early-life stress and of inflammation. Furthermore, there are overlapping trans-diagnostic patterns of association of childhood trauma and inflammation with clinical outcomes. These findings suggest new strategies to remediate the effect of childhood trauma before the onset of clinical symptoms, such as anti-inflammatory interventions and potentiation of adaptive immunity. Similar strategies might be used to ameliorate the unfavorable treatment response described in psychiatric patients with a history of childhood trauma.

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Inflammation and clinical response to treatment in depression: A meta-analysis

Cited by 546 publications

References 67 publications

Therapeutic Implications of Brain–Immune Interactions: Treatment in Translation

Therapeutic Implications of Brain–Immune Interactions: Treatment in Translation

Low tumor necrosis factor‐α levels predict symptom reduction during electroconvulsive therapy in major depressive disorder

Psychoneuroimmunology of Early-Life Stress: The Hidden Wounds of Childhood Trauma?

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