Inflammation in Depression
Downloads
Depression is a chronic condition that imposes a substantial burden of disability globally. Three principal neurotransmitters (norepinephrine (NE), dopamine (DA), and serotonin (5-HT)) implicated the pathophysiology and treatment of depression. Clinical studies have found a signiï¬cant association between numerous pro-inflammatory cytokines with depressive symptoms, endocrine, and neurotransmitter systems. Here, we detail our current understanding about the role of inflammation in depression, the mechanisms that are involved, and show how it is possible to innovate and develop new therapeutics of depression in the ï¬eld of neuroinflammation.
Kementerian Kesehatan Republik Indonesia, "HASIL UTAMA RISKESDAS 2018, Kementerian Kesehatan,” Ris. Kesehat. Dasar 2018, pp. 1–126, 2018.
K. L. L. Celina and S. Liu, Alexander Adibfar, Nathan Herrmann, Damien Gallagher, "Evidence for Inflammation-Associated Depression,” Evid. Inflammation-Associated Depress., no. November 2011, pp. 289–320, 2016, doi: 10.1007/7854.
Angelos Halaris, "Inflammation-Associated Co-morbidity Between Depression and Cardiovascular Disease,” Curr Top. Behav Neurosci, no. 2016, pp. 1–26, 2016, doi: 10.1007/7854_2016_28.
Z. M. Ignácio, R. S. da Silva, M. E. Plissari, J. Quevedo, and G. Z. Réus, "Physical Exercise and Neuroinflammation in Major Depressive Disorder,” Mol. Neurobiol., vol. 56, no. 12, pp. 8323–8335, 2019, doi: 10.1007/s12035-019-01670-1.
F. M. Syamsulhadi M., "CONSULTATION LIAISON PSYCHIATRY,” pp. 1–73, 2008.
A. B. and W. C. Drevets, "Role of Neuro-Immunological Factors in the Pathophysiology of Mood Disorders: Implications for Novel Therapeutics for Treatment Resistant Depression,” Brain Imaging Behav. Neurosci., no. November 2011, pp. 289–320, 2012, doi: 10.1007/7854.
S. M. Stahl, Stahl's Essential Psychopharmacology 4th Edition, vol. 53, no. 9. 2019.
J. C. Felger, "The Role of Dopamine in Inflammation- Associated Depression: Mechanisms and Therapeutic Implications,” Curr Top. Behav Neurosci, no. November 2011, pp. 289–320, 2012, doi: 10.1007/7854.
Andrew H. Miller and and Charles L. Raison, "The Role of Inflammation in Depression: From Evolutionary Imperative to Modern Treatment Target,” Nat. Rev. Immunol., vol. 16, no. 1, pp. 22–34, 2015, doi: 10.1038/nri.2015.5.
A. Suzumura and K. Ikenaka, Neuron-Glia Interaction in Neuro- in ammation. 2013.
Charlotte D'Mello and Mark G. Swain, "Immune-to-Brain Communication Pathways in Inflammation-Associated Sickness and Depression Charlotte,” Curr Top. Behav Neurosci, no. November 2011, pp. 289–320, 2012, doi: 10.1007/7854.
Stephen M. Stahl, Stahl Essential Psychopharmacology. 2016.
L. D. Godoy, M. T. Rossignoli, P. Delfino-Pereira, N. Garcia-Cairasco, and E. H. de L. Umeoka, "A comprehensive overview on stress neurobiology: Basic concepts and clinical implications,” Front. Behav. Neurosci., vol. 12, no. July, pp. 1–23, 2018, doi: 10.3389/fnbeh.2018.00127.
C. Kraus, E. Castrén, S. Kasper, and R. Lanzenberger, "Serotonin and neuroplasticity – Links between molecular, functional and structural pathophysiology in depression,” Neurosci. Biobehav. Rev., vol. 77, pp. 317–326, 2017, doi: 10.1016/j.neubiorev.2017.03.007.
N. A. Harrison, "Brain Structures Implicated in Inflammation-Associated Depression,” Brain Imaging Behav. Neurosci., no. November 2011, pp. 289–320, 2012, doi: 10.1007/7854.
J. F. S. Karol Ramirez, and Jaime Fornaguera-Trı´as, "Stress-Induced Microglia Activation and Monocyte Trafficking to the Brain Underlie the Development of Anxiety and Depression,” Curr Top. Behav Neurosci, no. November 2011, pp. 289–320, 2012, doi: 10.1007/7854.
M. A. Calcia, D. R. Bonsall, P. S. Bloomfield, S. Selvaraj, T. Barichello, and O. D. Howes, "Stress and neuroinflammation: A systematic review of the effects of stress on microglia and the implications for mental illness,” Psychopharmacology (Berl)., vol. 233, no. 9, pp. 1637–1650, 2016, doi: 10.1007/s00213-016-4218-9.
L. Wang, R. Wang, L. Liu, D. Qiao, D. S. Baldwin, and R. Hou, "Effects of SSRIs on peripheral inflammatory markers in patients with major depressive disorder: A systematic review and meta-analysis,” Brain. Behav. Immun., vol. 79, no. February, pp. 24–38, 2019, doi: 10.1016/j.bbi.2019.02.021.
Christopher R. Pryce and Adriano Fontana, "Depression in Autoimmune Diseases,” Curr Top. Behav Neurosci, no. November 2011, pp. 289–320, 2012, doi: 10.1007/7854.
G. E. Hodes, C. Ménard, and S. J. Russo, "Integrating Interleukin-6 into depression diagnosis and treatment,” Neurobiol. Stress, vol. 4, pp. 15–22, 2016, doi: 10.1016/j.ynstr.2016.03.003.
B. T. Baune, "Are Non-steroidal Anti-Inflammatory Drugs Clinically Suitable for the Treatment of Symptoms in Depression-Associated Inflammation?,” Curr Top. Behav Neurosci, 2016.
J. Savitz, "Role of Kynurenine Metabolism Pathway Activation in Major Depressive Disorders,” Brain Imaging Behav. Neurosci., no. November 2011, pp. 289–320, 2012, doi: 10.1007/7854.
Robert Dantzer, Inflammation-Associated Depression : Evidence , Mechanisms and Implications, 31st ed. USA: Springer International Publishing, 2017.
Charles L. Raison, "The Promise and Limitations of Anti-Inflammatory Agents for the Treatment of Major Depressive Disorder,” Curr Top. Behav Neurosci, 2016.
P. Zhang, L. Mo, X. Li, Q. Wang, and M. Tusconi, "Psychological intervention and its immune effect in cancer patients: A meta-analysis,” Med. (United States), vol. 98, no. 38, 2019, doi: 10.1097/MD.0000000000017228.
R. S. Opie et al., "Dietary recommendations for the prevention of depression,” Nutr. Neurosci., vol. 20, no. 3, pp. 161–171, 2017, doi: 10.1179/1476830515Y.0000000043.
R. Dantzer, In ammation-Associated Depression : Evidence , Mechanisms and Implications. .
B. T. Baune, "Are Non-steroidal Anti-Inflammatory Drugs Clinically Suitable for the Treatment of Symptoms in Depression-Associated Inflammation,” Brain Imaging Behav. Neurosci., no. November 2011, pp. 289–320, 2012, doi: 10.1007/7854.
Copyright (c) 2021 Novi Agung Rahmawati, Azimatul Karimah, Mustafa M Amin
This work is licensed under a Creative Commons Attribution-ShareAlike 4.0 International License.
1. Copyright of this journal is possession of the Author, by the knowledge of the Editorial Board and Journal Manager, while the moral right of the publication belongs to the author.
2. The journal allows the author(s) to retain publishing rights without restrictions.
3. The articles are published under a Creative Commons Attribution Share-Alike (CC BY-SA) license. Many research funding bodies prefer the CC BY-SA license because it allows for maximum dissemination and re-use of open access materials. Users are free to share (copy, distribute, and transmit) and remix (adapt) the contribution under this license, including for commercial purposes, as long as they attribute the contribution in the manner specified by the author or licensor.
