Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesis

Major depressive disorder affects approximately 8.4% of the United States population. The World Health Organization estimates that 280 million adults worldwide are suffering from depression. They have estimated that by 2030 it will be the second most serious condition. Current treatment relies on th...

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Main Authors: Irene Pastis, Melody G. Santos, Akshita Paruchuri
Format: Article
Language:English
Published: Frontiers Media S.A. 2024-01-01
Series:Frontiers in Behavioral Neuroscience
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fnbeh.2023.1282242/full
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author Irene Pastis
Melody G. Santos
Akshita Paruchuri
author_facet Irene Pastis
Melody G. Santos
Akshita Paruchuri
author_sort Irene Pastis
collection DOAJ
description Major depressive disorder affects approximately 8.4% of the United States population. The World Health Organization estimates that 280 million adults worldwide are suffering from depression. They have estimated that by 2030 it will be the second most serious condition. Current treatment relies on the monoamine hypothesis, however, one-third of patients with MDD do not respond to monoamine-based antidepressants. For years, it was hypothesized that the primary pathway of MDD involved serotonin as the main neurotransmitter. The monoamine hypothesis, a widely accepted theory, sought to explain the biological basis of MDD as being caused by the depletion of monoamine neurotransmitters, namely norepinephrine and serotonin. This hypothesis regarding monoamines as the pathophysiological basis of MDD led to the design and widespread use of selective serotonin reuptake inhibitors. However, given that only one-third of patients improve with SSRI it is reasonable to infer that the pathway involved is more complex than once hypothesized and there are more neurotransmitters, receptors, and molecules involved. The monoamine hypothesis does not explain why there is a delay in the onset of effect and action of SSRIs. Several studies have demonstrated that chronic stress is a risk factor for the development of MDD. Thus the monoamine hypothesis alone is not enough to fully account for the pathophysiology of MDD highlighting the need for further research involving the pathways of MDD. In this paper, we review the role of inflammation and cytokines on MDD and discuss other pathways involved in the development and persistence of depressive symptoms.
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spelling doaj.art-69ad63b469c24942ad65d96c596504a92024-01-17T12:37:12ZengFrontiers Media S.A.Frontiers in Behavioral Neuroscience1662-51532024-01-011710.3389/fnbeh.2023.12822421282242Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesisIrene Pastis0Melody G. Santos1Akshita Paruchuri2Department of Psychiatry and Behavioral Medicine, East Carolina University, Greenville, NC, United StatesInternal Medicine and Psychiatry Combined Program, Department of Psychiatry and Behavioral Medicine, East Carolina University, Greenville, NC, United StatesEast Carolina University Brody School of Medicine, Greenville, NC, United StatesMajor depressive disorder affects approximately 8.4% of the United States population. The World Health Organization estimates that 280 million adults worldwide are suffering from depression. They have estimated that by 2030 it will be the second most serious condition. Current treatment relies on the monoamine hypothesis, however, one-third of patients with MDD do not respond to monoamine-based antidepressants. For years, it was hypothesized that the primary pathway of MDD involved serotonin as the main neurotransmitter. The monoamine hypothesis, a widely accepted theory, sought to explain the biological basis of MDD as being caused by the depletion of monoamine neurotransmitters, namely norepinephrine and serotonin. This hypothesis regarding monoamines as the pathophysiological basis of MDD led to the design and widespread use of selective serotonin reuptake inhibitors. However, given that only one-third of patients improve with SSRI it is reasonable to infer that the pathway involved is more complex than once hypothesized and there are more neurotransmitters, receptors, and molecules involved. The monoamine hypothesis does not explain why there is a delay in the onset of effect and action of SSRIs. Several studies have demonstrated that chronic stress is a risk factor for the development of MDD. Thus the monoamine hypothesis alone is not enough to fully account for the pathophysiology of MDD highlighting the need for further research involving the pathways of MDD. In this paper, we review the role of inflammation and cytokines on MDD and discuss other pathways involved in the development and persistence of depressive symptoms.https://www.frontiersin.org/articles/10.3389/fnbeh.2023.1282242/fullmajor depressive disorderinflammationmonoamine hypothesisimmune pathwayscytokineskynurenine
spellingShingle Irene Pastis
Melody G. Santos
Akshita Paruchuri
Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesis
Frontiers in Behavioral Neuroscience
major depressive disorder
inflammation
monoamine hypothesis
immune pathways
cytokines
kynurenine
title Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesis
title_full Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesis
title_fullStr Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesis
title_full_unstemmed Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesis
title_short Exploring the role of inflammation in major depressive disorder: beyond the monoamine hypothesis
title_sort exploring the role of inflammation in major depressive disorder beyond the monoamine hypothesis
topic major depressive disorder
inflammation
monoamine hypothesis
immune pathways
cytokines
kynurenine
url https://www.frontiersin.org/articles/10.3389/fnbeh.2023.1282242/full
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