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The biology of depression is the attempt to identify a biochemical origin of depression, as opposed to theories that emphasize psychological or situational causes. Scientific studies have found that different brain areas show altered activity in humans with major depressive disorder (MDD) . [ 1 ]
While depression is a complex condition with many factors involved, it is commonly attributed to an imbalance of several key monoamine neurotransmitters, including serotonin, dopamine and norepinephrine. This monoamine hypothesis of depression is popular because of the simplicity of the explanation. [4]
The exact cause of catatonic depression is not fully understood. [1] However, it is believed to arise from a complex interplay of genetic, biochemical, and environmental factors. Some research suggests that disturbances in neurotransmitters like dopamine and gamma-aminobutyric acid (GABA) may contribute to the development of catatonic symptoms. [2]
Major depression was the leading cause of disease burden in North America and other high-income countries, and the fourth-leading cause worldwide as of 2006. In the year 2030, it is predicted to be the second-leading cause of disease burden worldwide after HIV , according to the WHO. [ 281 ]
The neurotrophic hypothesis of depression [1] proposes that major depressive disorder (MDD) is caused, at least partly, by impaired neurotrophic support.Neurotrophic factors (also known as neurotrophins) are a family of closely related proteins which regulate the survival, development, and function of neurons in both the central and peripheral nervous systems.
[12] [13] [14] One interpretation is that depression manifests due to an imbalance of neurotransmitters in the brain, resulting in feelings of worthlessness and despair. Magnetic resonance imaging shows that the brains of people diagnosed with depression may have a hippocampus up to 10% smaller than those who do not exhibit signs of depression.
Researchers theorized that depression was caused by a chemical imbalance in neurotransmitters in the brain, a theory based on observations made in the 1950s of the effects of reserpine and isoniazid in altering monoamine neurotransmitter levels and affecting depressive symptoms. [89]
[7] [65] Due to this sensitivity and NLPR3's role in triggering cytokine release, NLPR3 is thought to be a key component in sterile inflammatory responses, [7] something which has led to the suggestion that it is a likely mechanism linking non-pathogen induced stress to the increased inflammation that is common in depression and other forms of ...
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