Journals / Psikiyatride Güncel Yaklaşımlar / 2014 / Cilt: 6 - Sayı: 1

Neuroinflammatory Hypothesis in Major Depressive Disorder

Major Depresif Bozuklukta Nöroinflamatuvar Hipotez

Pages
1–9
Publication Date
2014-11-06
DOI
—
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AI Summary & Key Takeaways

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

In this article, the changes that occur in inflammatory processes in depressive disorder will be summarized; the effects of pharmacologic and psychotherapeutic approaches on these changes will be reviewed.

📌 3 Key Takeaways

🎯
Objective & Hypothesis:Faced with stress and acute instances, brain cells trigger neuroinflammation and increase inflam-mation response and can cause cell damage, cell death and thereby functional insufficiencies, behavioral disorders and autonomic imbalances.
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Key Findings & Data:It has been proven that inflammatory activity increases in depression.
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Conclusion & Impact:In this article, the changes that occur in inflammatory processes in depressive disorder will be summarized; the effects of pharmacologic and psychotherapeutic approaches on these changes will be reviewed.
🔬Design:Review & Systematic Survey
📍Scope:Comprehensive Sample
⚙️Variables:Major depresif bozukluk · nöroinflamatuvar hipotez · tedavi

Abstract

Faced with stress and acute instances, brain cells trigger neuroinflammation and increase inflam-mation response and can cause cell damage, cell death and thereby functional insufficiencies, behavioral disorders and autonomic imbalances. Cytokines that play an important role in inflamma-tory processes affect neurotransmitter metabolism, neuroendocrine functions and synaptic plasticity. It has been proven that inflammatory activity increases in depression. Proinflammatory cytokines such as interleukin (IL)-1, IL-6 and tumor necrosis factor (TNF)-α along with acute phase reactants increase in depression. If the inflammatory response becomes chronic and cannot be balanced, inflammation and cytokines may cause behavioral symptoms and neuropsychiatric disorders such as major depression and anxiety disorders. In this article, the changes that occur in inflammatory processes in depressive disorder will be summarized; the effects of pharmacologic and psychotherapeutic approaches on these changes will be reviewed.

Özet

Beyin hücreleri stres ve akut olaylar karşısında nöroinflamasyonu tetikleyerek ve inflamasyon yanıtını arttırarak hücre hasarına, ölümüne ve dolayısıyla fonksiyonel yetersizliklere, davranışsal bozukluklara ve otonomik dengesizliklere yol açabilmektedir. İnflamatuvar süreçlerde önemli rol oynayan sitokinler nörotransmitter metabolizması, nöroendokrin işlevler ve sinaptik plastisiteyi etkilemektedir. Depresyonda inflamatuvar aktivitenin artmış olduğu kanıtlanmıştır. Depresyonda interlökin (IL)-1, IL-6 ve tümör nekroz faktör (TNF)-α gibi proinflamatuvar sitokinler ve akut faz reaktanları artmaktadır. Psikososyal stresörlere yanıt olarak ortaya çıkan bu immun değişiklikler geçicidir ve anti-inflamatuvar mekanizmalarla dengelenmektedir. Bununla birlikte, inflamatuvar yanıt kronikleşirse ya da dengelenemezse inflamasyon ve sitokinler davranışsal belirtilere ve major depresyon, anksiyete bozuklukları gibi nöropsikiyatrik hastalıklara yol açabilmektedir. Bu yazıda, major depresif bozuklukta inflamatuvar süreçlerde meydana gelen değişiklikler özetlenecek, farmakolojik ve psikoterapötik yaklaşımların bu değişiklikler üzerine etkileri gözden geçirilmiştir.

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Cite This Article

Sözeri-Varma, G. (2014). Neuroinflammatory Hypothesis in Major Depressive Disorder. Psikiyatride Güncel Yaklaşımlar, Cilt: 6 - Sayı: 1, 1–9. https://ajindex.com/articles/217481

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References (15)

  1. Capuron L, Miller AH. Immune system to brain signaling: neuropsychopharmacological implications. Pharmacol Ther 2011; 130:226-238.
  2. Raison CL, Cowles MK, Miller AH. Immune system and central nervous system interactions. In Kaplan&Sadock’s Comprehensive Textbook of Psychiatry, 9th edition (Eds BJ Sadock, VA Sadock, P Ruiz):175-197.
  3. Philadelphia, PA, Lippincott, Williams&Wilkins, 2009.
  4. Tuğlu C, Kara SH. Depresyon, sitokinler ve bağışıklık sistemi. Klinik Psikofarmakoloji Bülteni 2003; 13:142-150. Dinan TG. Inflammatory markers in depression. Curr Opin Psychiatry 2009; 22:32-36.
  5. Schiepers OJ, Wichers MC, Maes M. Cytokines and major depression. Prog Neuropsychopharmacol Biol Psychiatry 2005; 29:201-217.
  6. Gümrü S, Arıcıoğlu F. Inflammation in depression: the role of cytokines. Marmara Üniversitesi Sağlık Bilimleri Enstitüsü Dergisi 2012; 2:103-107.
  7. Krishnadas R, Cavanagh J. Depression: an inflammatory illness? J Neurol Neurosurg Psychiatry 2012; 83:495-502. Raedler TJ. Inflammatory mechanisms in major depressive disorder. Curr Opin Psychiatry 2011; 24:519–525.
  8. Janssen DG, Caniato RN, Verster JC, Baune BT. A psychoneuroimmunological review on cytokines involved in antidepressant treatment response. Hum Psychopharmacol 2010; 25: 201-215.
  9. Howren MB, Lamkin DM, Suls J. Associations of depression with C-reactive protein, IL-1, and IL-6: a meta-analysis. Psychosom Med 2009; 71:171-186.
  10. Dowlati Y, Herrmann N, Swardfager W, Liu H, Sham L, Reim EK et al. A meta-analysis of cytokines in major depression. Biol Psychiatry 2010; 67:446-457.
  11. Duivis HE, Vogelzangs N, Kupper N, de Jonge P, Penninx BW. Differential association of somatic and cognitive symptoms of depression and anxiety with inflammation: findings from the Netherlands Study of Depression and Anxiety (NESDA). Psychoneuroendocrinology 2013; 38:1573-1585.
  12. Kocabaşoğlu N, Konuk N, Öztürk S, Bayar R. Akut faz proteinleri, immünite ve depresyon ilişkisi üzerine kontrollü bir çalışma. Yeni Symposium 2000; 36:83-87.
  13. Hocaoğlu Ç, Kural B, Aliyazıcıoglu R, Deger O, Cengiz S. IL-1 β, IL-6, IL-8, IL-10, IFN- γ, TNF- α and its relationship with lipid parameters in patients with major depression. Metab Brain Dis 2012; 27:425 -4 Doksat MK. Evrimsel perspektiften depresyon ve sitokinler. Klinik Psikofarmakoloji Bülteni 2003; 13:97-108.
  14. 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.
  15. Jones KA, Thomsen C. The role of t