The Effect of Newer Serotonin-Noradrenalin Antidepressants on Cytokine Production: A Review of the Current Literature

Berardis, Domenico De; Conti, Chiara; Serroni, Nicola; Moschetta, Francesco Saverio; Olivieri, Luigi; Carano, Alessandro; Salerno, Rosa Maria; Cavuto, Marilde; Farina, B.; Alessandrini, Marco; Janiri, Luigi; Pozzi, Gino; Giannantonio, Massimo Di

doi:10.1177/039463201002300204

Cited by 67 publications

(48 citation statements)

References 31 publications

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“…In these conditions the inflammatory processes rather than the medication might lead to depressive behaviour [78,79]. Indeed, both pre-clinical and clinical studies have demonstrated that newer serotonin-noradrenalin antidepressants can inhibit the production and release of pro-inflammatory cytokines and stimulate the production of anti-inflammatory cytokines [80]. Reductions in inflammation might therefore contribute to treatment response [80].…”

Section: Depression As An Inflammatory Disordermentioning

confidence: 99%

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Lang

Borgwardt²

2013

Cell Physiol Biochem

6,215

229

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Depression is a multicausal disorder and has been associated with the risk to develop cancer, dementia, diabetes, epilepsy and stroke. As a metabolic disorder depression has been associated with obesity, diabetes, insulin sensitivity, neuropeptide Y, glucose regulation, poor glycemic control, glucagone-like peptide-1, cholezystokinin, ghrelin, leptin, the endocannabinoid system, insulin-like growth factor and gastrin-releasing peptide. As a cardiovascular disease a close relationship exists between depression and blood pressure, heart rate, norepinephrine, sympathetic tone, vascular resistance, blood viscosity, plasma volume, intima thickness and atherosclerosis. Additionally blood coagulation, fibrinolysis, D-dimers, plasminogen activator inhibitor-1 protein, platelet activation, VEGF, plasma nitric oxide and its synthase are changed in depressed patients. As an endocrinological and stress disorder depression has been connected with the concentration of free T₄, TSH, CRH, arginine vasopressin, corticotrophin, corticosteroid release and ACTH. Depression as an inflammatory disorder is mediated by pro-inflammatory cytokines, interleukin-1, interleukin-6, TNF-alpha, soluble interleukin-2 receptors, interferon-alpha, interleukin 8, interleukin-10, hs-CRP, acute phase proteins, haptoglobin, toll like receptor 4, interleukin-1beta, mammalian target of rapamycin pathway, substance P, cyclooxygenase-2, prostaglandin-E2, lipid peroxidation levels and acid sphingomyelinase. Nutritional factors might influence depression risk, i.e. the consumption of folate, omega-3 fatty acids, monounsaturated fatty acids, olive oil, fish, fruits, vegetables, nuts, legumes, vitamin B6 and vitamin B12. The neurodegenerative hypothesis of depression explains decreased hippocampal volumes in depressed patients and changes of neurotrophic support by BDNF, erythropoietin, GDNF, FGF-2, NT3, NGF and growth hormone. In this context, a fast neuroprotective and antidepressant effect has also been observed by ketamine, which acts via the glutamatergic system. Hence, GABA, AMPA, EAAT, NMDA- and metabotropic glutamate receptors (mGluR1 to mGluR8) have gained interest in depression recently. Alternative, causative or also easy available treatment strategies beyond serotonin and noradrenaline reuptake inhibition might be a major topic of future psychiatric care. In this review, an attempt is made to overview concepts of the disease and search for perspectives on antidepressant treatment strategies beyond approved medications.

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Section: Depression As An Inflammatory Disordermentioning

confidence: 99%

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Lang

Borgwardt²

2013

Cell Physiol Biochem

6,215

229

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“…Several antidepressants have demonstrated some degree of efficacy in the treatment of ADs (4). Of these, SSRIs, SNRIs, and NaSSAs are currently preferred, being generally safer and better tolerated than TCAs or MAOIs (I).…”

mentioning

confidence: 99%

Is There a Role for Agomelatine in the Treatment of Anxiety Disorders? A Review of Published Data

Berardis¹,

Conti

Marini³

et al. 2013

Int J Immunopathol Pharmacol

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Anxiety disorders (ADs) are the most common type of psychiatric disorders. Pharmacologic options studied for treating ADs may include benzodiazepines, tricyclic antidepressants (TCA), selective serotonin reuptake inhibitors (SSRIs), noradrenergic and specific serotonergic antidepressants (NaSSA) and serotonin and noradrenaline reuptake inhibitors (SNRIs). Agomelatine, a new melatonergic antidepressant, has been shown effective in various types of mood disorders. Moreover, some evidence points towards a possible efficacy of such a drug in the treatment of ADs. Therefore, the aim of this review was to elucidate current (facts and views) data on the role of agomelatine in the treatment of ADs. The trials evaluating agomelatine in the treatment of generalized anxiety disorder are few but, overall, encouraging in regards to its efficacy. However, further randomized, placebo-controlled studies on larger samples use are needed. Apart from some interesting case reports, no large studies are, to date, present in literature regarding agomelatine in the treatment of other ADs, such as panic disorder, social anxiety disorder, obsessive-compulsive disorder and post-traumatic stress disorder. Therefore, the clinical efficacy and the relative good tolerability of agomelatine in generalized anxiety (GAD) warrants further investigation in ADs.

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“…It does not block the monoamine oxidase types A or B [53] . DUL has the capability to block the production and/or release of pro-inflammatory cytokines and/or can also provoke the production of anti-inflammatory cytokines [54] . DUL has properties for the modulation of nitroxidative stress by influencing the balance between pro-oxidant and anti-oxidant processes [55] .…”

Section: Duloxetine (Dul)mentioning

confidence: 99%

Alleviation of pain in painful diabetic neuropathy

Tajti

Delia

Majláth

et al. 2016

Expert Opinion on Drug Metabolism & Toxicology

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Introduction: Painful diabetic neuropathy (PDN) is a disabling pain condition. Its pathomechanism remains unknown, but a sensitization and neuronal hyperexcitabilty have been suggested. Only symptomatic pharmacological pain-alleviation treatment is currently available. Areas covered:The origin of PDN is enigmatic, and the evidence-based therapeutic guidelines therefore consist only of antidepressants and antiepileptics as first-line recommended drugs. This article relates to a MEDLINE/PubMed systematic search (2005)(2006)(2007)(2008)(2009)(2010)(2011)(2012)(2013)(2014)(2015). Expert opinion:The results of the meta-analysis from the aspect of the efficacy of amitriptyline, duloxetine, venlafaxine, gabapentin and pregabalin are favorable, but the placebo response rate is relatively high in patients with neuropathic pain. For personalization of the medication of PDN patients, the optimum dosing, the genotyping of the metabolizing enzymes and optimum biomarkers are needed. As concerns the future perspectives, specific sodium channel subtype inhibitors acting on peripheral nociceptive neurons or modified Ttype voltage-gated calcium channel blockers may be promising targets for pharmaceutical innovations. Another attractive strategy for the treatment is based on the effects of monoclonal antibodies against nerve growth factor, sodium channel, specific receptor and cytokines. Botulinum toxin A, capsaicin patch and spinal cord stimulation therapies are the nearest future therapeutic options for the treatment of PDN patients.

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The Effect of Newer Serotonin-Noradrenalin Antidepressants on Cytokine Production: A Review of the Current Literature

Cited by 67 publications

References 31 publications

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Molecular Mechanisms of Depression: Perspectives on New Treatment Strategies

Is There a Role for Agomelatine in the Treatment of Anxiety Disorders? A Review of Published Data

Alleviation of pain in painful diabetic neuropathy

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