Potential Involvement of Mitochondrial Dysfunction in Major Depressive Disorder: Recent Evidence
Archives of Depression and Anxiety
Mini Review
Abstract
Major depressive disorder (MDD) is a leading cause of morbidity and mortality, and it is a common psychological disorder in the world. Present antidepressants modulate monoamine systems directly or indirectly, because MDD is classically considered as a neurochemical disease, in which monoamine systems are perturbed including serotonin, noradrenaline or dopamine systems. However, recent evidences suggest that MDD is associated with the impairments of synaptic plasticity or cellular resilience to stress. Cellular resilience is maintained by mitochondria with the supplying cellular fuel or ATP. In addition, it is suggested that mitochondrial functions in neurons influence synaptic plasticity. Therefore, impairment of mitochondrial function can be the cause of the MDD. The present review article summarizes the recent evidences about the association between mitochondrial impairment and MDD, and it suggests that improvement of mitochondrial function become a potential drug target for MDD.
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Mini Review
Abstract
Major depressive disorder (MDD) is a leading cause of morbidity and mortality, and it is a common psychological disorder in the world. Present antidepressants modulate monoamine systems directly or indirectly, because MDD is classically considered as a neurochemical disease, in which monoamine systems are perturbed including serotonin, noradrenaline or dopamine systems. However, recent evidences suggest that MDD is associated with the impairments of synaptic plasticity or cellular resilience to stress. Cellular resilience is maintained by mitochondria with the supplying cellular fuel or ATP. In addition, it is suggested that mitochondrial functions in neurons influence synaptic plasticity. Therefore, impairment of mitochondrial function can be the cause of the MDD. The present review article summarizes the recent evidences about the association between mitochondrial impairment and MDD, and it suggests that improvement of mitochondrial function become a potential drug target for MDD.
http:
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