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<h2 id ="Subtitle1">Background</h2> | <h2 id ="Subtitle1">Background</h2> | ||
− | <p> Exposure to prolonged chronic stress induces heightened vulnerability to anxiety, depression, and | + | <p> According to the World Health Organization (WHO), depression is becoming the leading cause of disability worldwide, affecting more than 264 million people worldwide<sup>[<a href="#ref1">1</a>]</sup>. |
− | + | <p> Exposure to prolonged chronic stress induces heightened vulnerability to anxiety, depression, and several mood disorders. Chronic stress-induced depression (CSID) is characterized by the dysfunction of the medial prefrontal cortex (mPFC) in the brain, linked to cognitive and emotional deficiencies induced by long-term stress exposure<sup>[<a href="#ref2">2</a>]</sup>.</p> | |
+ | <p> Research has shown that chronic stress is closely related to the dysregulation of the gut-brain axis. In addition, gut-modifying substances, such as immune-inflammatory cytokines and Reactive oxygen species (ROS), cause detrimental effects on the gute<sup>[<a href="#ref3">3</a>]</sup>. The immune-inflammatory and oxidative stress pathways will be further discussed in the following sections.</p> | ||
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<h3>Immune-inflammatory Pathway in Depression</h3> | <h3>Immune-inflammatory Pathway in Depression</h3> | ||
− | <p> Interferon-gamma (IFN-γ) | + | <p> <b>Interferon-gamma (IFN-γ) is known to be positively correlated with depressive symptoms<sup>[<a href="#ref4">4</a>]</sup></b>. Research indicates that the activation of immune-inflammatory pathways and neural-immune interactions are closely involved in the pathophysiology of depressive disorders.</p> |
− | + | <p> Below are two immune-inflammatory pathways :</p> | |
− | + | <ol> | |
− | + | <li><b>Higher serum levels of inflammatory cytokines.</b><br>interleukin-6 (IL-6), IL-1β, and TNF-α could cause depressive disorders by disrupting neurotransmitter synthesis and signal transduction.</li> | |
− | + | <li><b>T-cell abnormal activation.</b><br>Elevated serum levels of neopterin, as well as activation of Th1-like and Th-17-like cells, including increased production of IL-2 and IFN-γ, will activate more inflammatory cytokines production.</li> | |
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− | </ | + | </ol> |
− | + | <h3>Oxidative Stress Pathway in Depression</h3> | |
− | + | ||
<p> The intracellular biological imbalance between ROS (reactive oxygen species) and antioxidants, leading to the alteration of biomolecules and the dysregulation of redox signaling pathways, is known to be OS. Both neuronal OS and intestinal OS could lead to the occurrence of CSID. Followings are physiological damages inflicted by excessive ROS<sup>[<a href="#ref3">3</a>]</sup>:</p> | <p> The intracellular biological imbalance between ROS (reactive oxygen species) and antioxidants, leading to the alteration of biomolecules and the dysregulation of redox signaling pathways, is known to be OS. Both neuronal OS and intestinal OS could lead to the occurrence of CSID. Followings are physiological damages inflicted by excessive ROS<sup>[<a href="#ref3">3</a>]</sup>:</p> | ||
<ul> | <ul> |
Revision as of 13:22, 19 October 2021