[Mitochondrial factor expression changes as a molecular basis of CNS disorders]

Mitochondrial dysfunction has been increasingly recognised as a key contributor to the pathophysiology of central nervous system disorders. Traditionally, mitochondrial abnormalities have been attributed primarily to structural defects caused by mutations in nuclear or mitochondrial DNA. However, accumulating evidence indicates that mitochondrial dysfunction is also widely observed in disorders such as autism spectrum disorder (ASD), major depressive disorder (MDD), and Parkinson's disease (PD), even in the absence of identifiable mitochondrial gene mutations. These findings suggest that mitochondrial impairment may arise through dysregulation of dynamic cellular and environmental response systems rather than through genetic defects alone. In this review, we discuss mitochondrial function as a dynamically regulated and environmentally responsive system involved in the maintenance of neural homeostasis. We focus on the effects of nutritional and metabolic environments on oligodendrocyte function in ASD, stress-associated mitochondrial regulation in MDD, and the role of the complex I regulatory factor p13 in PD. We further summarise how alterations in mitochondrial regulation contribute to disease-specific abnormalities in neural circuits and cellular function. Collectively, these findings support the concept that mitochondrial dysfunction in central nervous system disorders should be understood not only as a consequence of genetic abnormalities, but also as a disruption of functional regulation mediated by environmental factors and intracellular signalling pathways.