Proper functioning of the central nervous system (CNS) requires a tremendous amount of energy and any disturbance in mitochondrial homeostasis can result in disruptions in crosstalk among cells in the CNS. Traumatic CNS injury triggers a series of complex secondary pathophysiological processes that culminate in significant changes in cellular energy metabolism. In this context, mitochondrial medicine is an emerging field addressing mitochondrial dysfunction and uncoupling, including reactive oxygen/nitrogen species release, aberrant calcium flux and glutamate excitotoxicity. Changes in mitochondrial biogenesis, mitophagy and mitochondrial transfer among cells contributes significantly to functional outcome post-injury, and compromised bioenergetics of supporting cells exacerbates neuronal injury that further mitigates recovery. In addition to maintaining mitochondrial bioenergetics, pharmacologically, recent data show that after CNS injury mitochondria can be released from cells and transferred to neighboring compromised cells. Whether this transfer has positive or negative effects on recipient cells and consequent functional recovery is a burgeoning field of investigation. Accordingly, this session will consist of experts who will discuss mitochondrial contributions to both pathophysiology as well as reparative responses after CNS injury in relation to a wide range of models and functional outcomes for potential therapeutic applications of mitochondrial medicine.
At the conclusion of this session, attendees will be able to: