SavedAdd your journal

Journals / Clinical and Experimental Health Sciences / 2012 / Cilt: 2 - Sayı: 3

Inflammation in depression: the role of cytokines

Depresyonda inflamasyon: sitokinlerin rolü

Salih Gümrü
Feyza Arıcıoğlu
Pages
103–107
Publication Date
2014-01-30
DOI
—
🏛️Bibliographic metadata and full text access for this article are provided via DergiPark.
DergiPark Record ↗
✨

AI Summary & Key Takeaways

AI Insight
⚡ TL;DR(Too Long; Didn't Read)

The new hypothesis of depression provided some new opportunities in treatment of depression.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Recent studies support the concept that inflammatory mechanisms play a crucial role in the pathomechanisms of major depression.
📊
Key Findings & Data:Major depression shares similarities with ‘sickness behavior’, a normal response to inflammatory cytokines.
💡
Conclusion & Impact:The new hypothesis of depression provided some new opportunities in treatment of depression.
🔬Design:Research Article
📍Scope:Comprehensive Sample
⚙️Variables:Sitokin · inflamasyon · depresyon

Abstract

Recent studies support the concept that inflammatory mechanisms play a crucial role in the pathomechanisms of major depression. Major depression shares similarities with ‘sickness behavior’, a normal response to inflammatory cytokines. Elevations in proinflammatory cytokines and other inflammation-related proteins in major depression were found in plasma and cerebrospinal fluid (CSF). Clinical progress of the disease may also be predicted by the changes in proinflammatory cytokine levels. Antidepressant treatment can lead to a normalization of elevated cytokine levels in major depression. The new hypothesis of depression provided some new opportunities in treatment of depression.

Özet

Son yıllarda yapılan çalışmalar majör depresyonun patolojisinde inflamatuvar mekanizmaların önemli rol oynadığını göstermektedir. Majör depresyonda, inflamatuvar sitokinlere verilen yanıt olan “hastalık davranışı”na benzer belirtiler görülmektedir. Depresif hastaların plazma ve beyin omurilik sıvılarında proinflamatuvar sitokinler ve inflamasyonla bağlantılı proteinlerin miktarında artış gözlenir. Hastalığın prognozu da sitokin değerlerindeki değişmelerle paralellik göstermektedir. Antidepresan tedavi ile sitokin seviyeleri normale çevrilebilmektedir. Depresyonun bu yeni hipotezi, tedavide de yenilikleri gündeme getirmiştir.

🔖

Cite This Article

Gümrü, S., Arıcıoğlu, F. (2014). Inflammation in depression: the role of cytokines. Clinical and Experimental Health Sciences, Cilt: 2 - Sayı: 3, 103–107. https://ajindex.com/articles/481850

📄 Full Text PDF Viewer

📄

PDF görüntüleyici hazırlanıyor...

References (9)

  1. Maes M. Evidence for an immune response in major depression: a review and hypothesis. Prog Neuropsychopharmacol Biol Psychiatry. 1995;19(1):11–38. Maes M. The immune pathophysiology of major depression. Depression: Neurobiological, Psychopathological and Therapeutic Advances. 1st ed. London: John Wiley; 1997. p. 197-215.
  2. Raison CL, Capuron L, Miller AH. Cytokines sing the blues: Inflammation and the pathogenesis of major depression. Trend Immunol. 2006;27:24-31.
  3. Maes M, Galecki P, Chang YS, Berk M. A review on the oxidative and nitrosative stress (O&NS) pathways in major depression and their possible contribution to the (neuro)degenerative processes in that illness. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):676- 692. Maes M, Leonard BE, Myint AM, Kubera M, Verkerk R. The new ‘5-HT’ hypothesis of depression: cell-mediated immune activation induces indoleamine 2,3-dioxygenase, which leads to lower plasma tryptophan and an increased synthesis of detrimental tryptophan catabolites (TRYCATs), both of which contribute to the onset of depression. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):702-721.
  4. Song C, Wang H. Cytokines mediated inflammation and decreased neurogenesis in animal models of depression. 2011;35(3):760-768.
  5. Kubera M, Obuchowicz E, Goehler L, Brzeszcz J, Maes M. In animal models, psychosocial stress-induced (neuro)inflammation, apoptosis and reduced neurogenesis are associated to the onset of depression. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):744-759.
  6. Maes M, Leonard B, Fernandez A, Kubera M, Nowak G, Veerhuis R, Gardner A, Ruckoanich P, Geffard M, Altamura C, Galecki P, Berk M. Editorial: (Neuro)inflammation and neuroprogression as new pathways and drug targets in depression: From antioxidants to kinase inhibitors. Prog Neuropsychopharmacol Biol Psychiatry. 2011;35(3):659-663.
  7. Miller AH, Maletic V, Raison CL. Inflammation and its discontents: The role of cytokines in the pathophysiology of major depression. Biol Psychiatry. 2009;65:732-741.
  8. Khairova RA, Machado-Vieira R, Du J, Manji HK. A potential role for pro-inflammatory cytokines in regulating synaptic plasticity in major depressive disorder. Int J Neuropsychopharmacol. 2009;12(4):561- 578. Sommer N, Löschmann PA, Northoff GH, Weller M, Steinbrecher JP, Lichtenfels R, Meyermann R, Riethmüller A, Fontana A. The antidepressant rolipram suppresses cytokine production and prevents autoimmune encephalomyelitis. Nature Medicine. 1995;1:244-248.
  9. Navikas V, Matusecicu