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The Role of Glial Pathology in Pathophysiology and Treatment of Major Depression: Clinical and Preclinical Evidence

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Translational Research Methods for Major Depressive Disorder

Part of the book series: Neuromethods ((NM,volume 179))

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Abstract

Major depressive disorder is the most common neuropsychiatric disorder affecting millions of people worldwide, with severe consequences and causing the greatest loss of workforce. The monoamine hypothesis is still valid in explaining the etiopathogenesis of depression. Current treatment approaches aim to change the monoamine levels in the synaptic space with various mechanisms of action. However, relapse rates could not be significantly reduced with antidepressant drugs developed and introduced in the last 50 years. The neuroinflammation hypothesis comes to the fore as a solution alternative to these treatment searches stuck in the synaptic gap. One of the important pillars of neuroinflammation is glial dysfunction. Studies investigating cytokine, interleukin, and brain-derived neurotrophic factor (BDNF) levels associated with microglia and astroglia cells are increasing. Antidepressant activity can be obtained, and new antidepressant drug candidates can be determined by means of ligands that agonize and antagonize the glial activity. In this article, clinical and preclinical studies on glial dysfunction in the etiopathogenesis of depression and the treatment approaches recommended on this basis are discussed.

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Evrensel, A., Tarhan, N. (2022). The Role of Glial Pathology in Pathophysiology and Treatment of Major Depression: Clinical and Preclinical Evidence. In: Kim, YK., Amidfar, M. (eds) Translational Research Methods for Major Depressive Disorder. Neuromethods, vol 179. Humana, New York, NY. https://doi.org/10.1007/978-1-0716-2083-0_2

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  • DOI: https://doi.org/10.1007/978-1-0716-2083-0_2

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  • Publisher Name: Humana, New York, NY

  • Print ISBN: 978-1-0716-2082-3

  • Online ISBN: 978-1-0716-2083-0

  • eBook Packages: Springer Protocols

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