ABSTRACT
Oxidative stress and mitochondrial dysfunction have been implicated in the pathogenesis of neurodegenerative diseases, including multiple sclerosis (MS). MS has been considered as a chronic, inflammatory disorder of the central nervous system in which ensuing demyelination and axonal damage that result in physical disability affecting over 2 million people worldwide. Mitochondrial dysfunction is distinguished by the overproduction of reactive oxygen species, which can induce the mitochondrial DNA mutations, disrupt the calcium ions homeostasis, impair mitochondrial respiratory chain and alter membrane permeability. Neurons are highly dependent on oxidative energy metabolism. Extreme production of free radicals leads to axonal injury, leukocyte migration and oligodendrocyte damage can be observed in MS patients. Importantly, all these changes are implicated in the development of mediating and/or amplifying neuronal dysfunction and triggering neurodegeneration. Therefore, more insight into the cause and consequences of impaired mitochondrial function provide a foundation for mitochondrial-targeted medicine to combat progressive MS.
