Role of cytokines in psychopathology: therapeutic implications.
TL;DR: Considering the human and economic costs of major psychiatric disorders, alteration of the cytokine network as a potential therapeutic tool is worthy of consideration and investigation.
Abstract: Cytokines can influence physiological functions such as sleep and food intake; they also interact with a number of neurotransmitters and second messengers in the brain. Cytokines are involved in a number of infectious, inflammatory, neoplastic, metabolic and degenerative illnesses. They also have been implicated in some psychiatric disorders, including 1) depressive and anxiety disorders; 2) schizophrenic disorders (chronic and acute); 3) autistic disorder; 4) eating disorders; and 5) obsessive-compulsive disorder. Alterations in cytokine peptide/receptor production or function in major psychiatric disorders are of special interest to researchers in the field. Exogenous administration of cytokines may be of therapeutic value in disorders in which the cytokine system may be disturbed. In some brain disorders of defined neuropathology, some cytokines have been found clinically useful. Such a development has yet to occur in the treatment of psychiatric disorders; however, some limited and very preliminary observations suggest that manipulation of the cytokine network may be of potential value in the treatment of some psychiatric disorders. Considering the human and economic costs of major psychiatric disorders, alteration of the cytokine network as a potential therapeutic tool is worthy of consideration and investigation.
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TL;DR: This trial suggests that N-acetylcysteine may be a safe and effective option to augment standard treatment in patients with refractory obsessive-compulsive disorder.
Abstract: ObjectiveThis study aimed to evaluate the efficacy and safety of N-acetylcysteine, a glutamate-modulating agent, in patients with treatment-refractory obsessive-compulsive disorder as an adjunct to serotonin reuptake inhibitor treatment.MethodsForty-eight patients (36 women; mean ± SD age, 30.93 ± 4
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TL;DR: It is demonstrated that ELS induced by LN conferred some metabolic protection against insulin and/or glucose intolerance in a diet-dependent manner during adulthood.
Abstract: Environmental conditions experienced in early life can profoundly influence long-term metabolic health, but the additive impact of poor nutrition is poorly understood. Here we tested the hypothesis that early life stress (ELS) induced by limited nesting material (LN) combined with high fat and high sugar diet (HFHS) post-weaning would worsen the diet-related metabolic risk. Sprague-Dawley female rats were exposed to LN, postnatal days 2-9, and at weaning (3 weeks), siblings were given unlimited access to chow or HFHS resulting in (Con-Chow, Con-HFHS, LN-Chow, LN-HFHS, n=11-15 per group). Glucose and insulin tolerance were tested and rats were killed at 13 weeks. LN rats weighed less at weaning but were not different to control at 13 weeks; HFHS diet led to similar increases in body weight. LN-chow rats had improved glucose and insulin tolerance relative to Con-Chow, whereas LN-HFHS exhibited improved insulin sensitivity versus Con-HFHS, associated with increased peroxisome proliferator-activated receptor gamma coactivator-1-alpha (pgc-1α) mRNA in muscle. No effect of LN on plasma or liver triglycerides was observed, and hepatic gluconeogenic regulatory genes were unaltered. In summary, this study demonstrates that ELS induced by LN conferred some metabolic protection against insulin and/or glucose intolerance in a diet-dependent manner during adulthood.
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