A potential role for pro-inflammatory cytokines in regulating synaptic plasticity in major depressive disorder

Khairova, Rushaniya; Machado‐Vieira, Rodrigo; Du, Jing; Manji, Husseini K.

doi:10.1017/s1461145709009924

Cited by 301 publications

(204 citation statements)

References 197 publications

(197 reference statements)

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“…We are, however, unable to examine the effect of in utero cigarette smoke exposure, which is a risk factor for both depression and asthma in the offspring (43,44). Depression is also associated with high systemic levels of inflammatory cytokines, particularly TNFa, which, in turn, has a pathogenic role in asthma (45,46). Finally, a potential neuroendocrine mechanism involves depression-related alteration in the hypothalamic-pituitary-adrenal axis that For definition of abbreviation, see Table 2.…”

Section: Discussionmentioning

confidence: 99%

Depression and Risk of Incident Asthma in Adults. The CARDIA Study

Brunner

Schreiner

Sood

et al. 2014

Am J Respir Crit Care Med

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Rationale: Asthma is associated with depression, but the temporality of the association has not been established.Objectives: To examine the association between prevalent elevated depressive symptoms and incident asthma, and between prevalent asthma and incident elevated depressive symptoms in a cohort of young and middle-aged adults.Methods: We examined the longitudinal association between asthma and depressive symptoms bidirectionally in the Coronary Artery Risk Development in Young Adults (CARDIA) cohort. First, 3,614 participants, free of asthma, were classified by elevated depressive symptoms at the CARDIA Year-5 exam (n = 856 elevated vs. 2,758 not elevated; ages 23-35 yr) and followed for 20 years to incident asthma. Then, 3,016 participants, free of elevated depressive symptoms, were classified by self-reported current asthma status (n = 188 prevalent vs. 2,828 not prevalent) at the CARDIA Year-5 exam and followed for 20 years until onset of elevated depressive symptoms. Measurements and Main Results:The relative hazard of incident asthma among those with elevated depressive symptoms was 1.26 (95% confidence interval [CI] = 1.02-1.56) after adjustment for covariates. When depressive status was modeled as the total number of reports of elevated depressive symptoms before the onset of asthma, the adjusted hazard ratio was 1.15 (95% CI = 1.02-1.29). The hazard of incident elevated depressive symptoms for those with asthma was no different than the hazard in those without asthma (adjusted hazard ratio = 0.92; 95% CI = 0.70-1.20).Conclusions: This longitudinal observational study points to depression as a marker of risk for incident adult-onset asthma. On the other hand, prevalent asthma is not associated with incident adultonset depression.

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Section: Discussionmentioning

confidence: 99%

Depression and Risk of Incident Asthma in Adults. The CARDIA Study

Brunner

Schreiner

Sood

et al. 2014

Am J Respir Crit Care Med

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“…Several studies have revealed that gene variants that contribute to an augmented inflammatory response are associated with the pathogenesis of many diseases including psychiatric disorders [36,37]. Independent genetic polymorphism (Table 2) and gene expression (Table 3) In addition, there is now evidence that receptors for the pro-inflammatory cytokines, such as TNF-α, IL-1β, IL-6 and the IFNs, are constitutively expressed in the hippocampus, thalamus, hypothalamus, dentate gyrus and cortex [90]. and infectious diseases and in several brain pathologies [91].…”

Section: Introductionmentioning

confidence: 99%

Recent advances in psychoneuroimmunology: Inflammation in psychiatric disorders

Debnath

Doyle

Langan

et al. 2011

Translational Neuroscience

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Psychiatric disorders are common and complex and their precise biological underpinnings remain elusive. Multiple epidemiological, molecular, genetic and gene expression studies suggest that immune system dysfunction may contribute to the risk for developing psychiatric disorders including schizophrenia, bipolar disorder, and major depressive disorder. However, the precise mechanisms by which inflammationrelated events confer such risk are unclear. In this review, we examine the peripheral and central evidence for inflammation in psychiatric disorders and the potential molecular mechanisms implicated including inhibition of neurogenesis, apoptosis, the HPA-axis, the role of brain-derived neurotrophic factor and the interplay between the glutamatergic, dopaminergic and serotonergic neurotransmitter systems.

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“…The increased production of proinflammatory cytokines and infiltration of peripheral immune cells into the central nervous system (CNS) are closely associated with neuronal damage in the spinal cord and many brain regions (6)(7)(8)(9)(10). Elevation of several cytokines such as TNF-α and IFN-γ precedes infiltration of peripheral immune cells and could have a significant impact on neuronal function (11)(12)(13)(14)(15)(16)(17)(18)(19), potentially contributing to early sensory and cognitive impairments. However, the link between the cytokine elevation and CNS deficits in autoimmune diseases remains unclear.…”

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confidence: 99%

Peripheral elevation of TNF-α leads to early synaptic abnormalities in the mouse somatosensory cortex in experimental autoimmune encephalomyelitis

Yang

Parkhurst

Hayes

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

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Sensory abnormalities such as numbness and paresthesias are often the earliest symptoms in neuroinflammatory diseases including multiple sclerosis. The increased production of various cytokines occurs in the early stages of neuroinflammation and could have detrimental effects on the central nervous system, thereby contributing to sensory and cognitive deficits. However, it remains unknown whether and when elevation of cytokines causes changes in brain structure and function under inflammatory conditions. To address this question, we used a mouse model for experimental autoimmune encephalomyelitis (EAE) to examine the effect of inflammation and cytokine elevation on synaptic connections in the primary somatosensory cortex. Using in vivo two-photon microscopy, we found that the elimination and formation rates of dendritic spines and axonal boutons increased within 7 d of EAE induction-several days before the onset of paralysis-and continued to rise during the course of the disease. This synaptic instability occurred before T-cell infiltration and microglial activation in the central nervous system and was in conjunction with peripheral, but not central, production of TNF-α. Peripheral administration of a soluble TNF inhibitor prevented abnormal turnover of dendritic spines and axonal boutons in presymptomatic EAE mice. These findings indicate that peripheral production of TNF-α is a key mediator of synaptic instability in the primary somatosensory cortex and may contribute to sensory and cognitive deficits seen in autoimmune diseases.

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A potential role for pro-inflammatory cytokines in regulating synaptic plasticity in major depressive disorder

Cited by 301 publications

References 197 publications

Depression and Risk of Incident Asthma in Adults. The CARDIA Study

Depression and Risk of Incident Asthma in Adults. The CARDIA Study

Recent advances in psychoneuroimmunology: Inflammation in psychiatric disorders

Peripheral elevation of TNF-α leads to early synaptic abnormalities in the mouse somatosensory cortex in experimental autoimmune encephalomyelitis

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