Multiple sclerosis is one of the most frequent chronic inflammatory diseases of the CNS. Progress has been made in understanding and moderating the acute inflammatory components, but the mechanisms of the concomitant neurodegeneration are still not understood. Clinical outcome is thought to depend on the balance between inflammation and the capacity for neuronal self-protection/regeneration. With the aim of identifying potential novel therapeutic targets, the authors review research on the mechanisms of neuroaxonal dysfunction and injury and the endogenous neuroprotective pathways that counteract oxidative stress and mitochondrial dysfunction. Mechanisms inherent to neurons and their axons, but separable from those acting on inflammatory responses may represent suitable neuroprotective drug targets with the capability to halt multiple sclerosis progression.
Friese MA, Schattling B, Fugger L: Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis. Nature Reviews Neurology 10(4): 225-238 (2014).
