Mitochondrial dysfunction is widely recognized as a hallmark of neurodegenerative disorders, such as Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and amyotrophic lateral sclerosis, as well as acute neurologic injuries, such as occur with ischemic stroke and traumatic brain injury. Recent studies have shown that mitochondrial transfer between cells may be an effective strategy for maintaining cell survival and treating neurologic diseases. This review summarizes the current research on the mechanisms underlying mitochondrial dysfunction and transfer in the central nervous system and the potential of mitochondrial transfer as a therapeutic strategy. The mechanisms and consequences of mitochondrial dysfunction are described first. Then, the mechanism underlying mitochondrial transfer is described. Subsequently, two complementary therapeutic approaches are critically evaluated: enhancing endogenous transfer pathways; and administering exogenous mitochondrial transplantation. Evidence from preclinical models of stroke, neurodegenerative diseases, and traumatic brain injury demonstrates that these strategies can improve neuronal survival and functional recovery. Lastly, to fully realize the potential of mitochondrial transplantation in the treatment of neurologic disorders, it is recommended that future research explore deeper into the molecular signaling pathways involved in the functional integration of mitochondria transfer and investigate ways to improve the efficiency of mitochondrial transplantation using donor cells, like mesenchymal stem cells.
Zhang et al. (Thu,) studied this question.