Depression and anxiety: Role of mitochondria

摘要

Depressive and anxiety disorders appear to share an underlying element of distress, forming a general class of mood disorders. The diagnosis of chronic stress-related disorders can be difficult because of non-specific symptoms being masked by other co-morbid states that may also be inadequately described by the patient. Co-morbidity with psychiatric disorders is common, especially in major depressive disorder. It is important to differentiate chronic and acute stress-related disorders, triggered by life events or stressors. Dysfunction in monoamine neurotransmitter systems have for the last 40 years remained the central model considered to play an important role in mediating the physiological and cognitive aspects of depression. The pharmacological action of antidepressants occurs within minutes to hours after administration, but the clinical effect and alleviation of symptoms can take 10-14 days following chronic administration. The discrepancy between pharmacological action and clinical relief of symptoms implies that monoamine depletion alone forming the underlying pathogenesis of depression may be oversimplified. Several neurotransmitters and neuropeptides play a role in the complex neuroanatomical pathways in anxiety. Complex intracellular cascades upregulated in stress-related disorders appear to be intimately associated with the metabolic integrity and capacity of mitochondria to maintain energetic parameters and ultimately cellular stability. Future therapeutic intervention may lie in understanding the interrelationship between hormonal, metabolic and molecular intracellular signaling pathways involved in these conditions. Thus, targeting mitochondrial function may represent a novel avenue for the development of therapies for the treatment of stress-related disorders.