Mitochondria act as central regulators of neuronal homeostasis by integrating energy metabolism with redox signaling, calcium balance, and cell fate determination. Neurons rely on oxidative phosphorylation to sustain synaptic transmission and plasticity and therefore are highly vulnerable to mitochondrial failure. When mitochondrial integrity is compromised, the resulting energy deficit, oxidative stress, and impaired quality control trigger a cascade of degenerative processes that culminate in neuronal death. Recent discoveries have demonstrated that mitochondria are not static organelles confined to individual cells but can be moved between cells through specialized intercellular pathways. This transfer allows damaged neurons to eliminate dysfunctional mitochondria or acquire healthy mitochondria from neighboring glial cells, thereby restoring bioenergetic function and promoting tissue repair. Here, we review current advances in understanding of mitochondrial function in the nervous system, the mechanisms and consequences of mitochondrial dysfunction, and emerging therapeutic strategies aimed at preserving or restoring mitochondrial integrity. We particularly emphasize the potential of intercellular mitochondrial transfer to reshape therapeutic approaches for neurological disease.
Ling et al. (Thu,) studied this question.