br Conclusions CK inhibition protects young and aging WM fun
Conclusions CK2 inhibition protects young and aging WM function against an ischemic episode by preserving oligodendrocytes and axonal structure by maintaining mitochondrial integrity. CK2 recruits CDK5 and AKT/GSK3ß signaling to mediate WM ischemic injury in a differential spatiotemporal manner such that CDK5 signaling becomes important during ischemia, while AKT signaling emerges as the main pathway during the reperfusion Salicylic acid following ischemia (Fig. 11). Subsequently, interventions selectively targeting the activated form of AKT confer post-ischemic functional recovery in young and aging WM. These findings warrant evaluation of the roles of CDK5 and AKT signaling in other WM-related diseases such as multiple sclerosis, traumatic brain injury, and spinal cord injury, as well as in neurodegenerative diseases such as Alzheimer\'s disease and in cerebral WM injury.
Declarations of interest