우울증의 병태생리 - 다요인적 메커니즘과 상호작용

Pathophysiology of depression : multifactorial mechanisms and interactions

Depression is a major mental health disorder that goes beyond mere emotional distress, significantly impairing daily life and social functioning. Without proper treatment, it can lead to severe consequences and currently affects hundreds of millions of people worldwide. The pathophysiology of depression arises from the complex interplay of biological, genetic, and environmental factors. Key mechanisms include imbalances in monoamine neurotransmitters (serotonin, norepinephrine, dopamine), dysfunction of the hypothalamic-pituitary-adrenal (HPA) axis, impaired neurogenesis, increased secretion of pro-inflammatory cytokines, and elevated levels of corticotropin-releasing hormone (CRH). Notably, the monoamine depletion hypothesis suggests that reduced availability of serotonin, norepinephrine, and dopamine in synaptic clefts can lead to depressive symptoms. Neuroendocrine abnormalities are also closely linked to depression. Elevated cortisol levels and impaired feedback regulation of the HPA axis are frequently observed in depressed patients. Additionally, excessive CRH secretion, decreased glucocorticoid receptor sensitivity, and altered growth hormone responses contribute to the worsening of depressive symptoms. The primary treatments currently used for depression are Selective Serotonin Reuptake Inhibitors (SSRIs) and Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs). However, these medications do not produce the same effects for all patients, and only a portion of individuals experience satisfactory therapeutic outcomes. By exploring how various factors interact to trigger and sustain depressive symptoms, this paper aims to contribute to the development of more effective and personalized treatment strategies and preventive measures.