Abstract:

Multiple sclerosis (MS) is a chronic disorder affecting central ner-vous system (CNS) in which inflammatory and neuro-degenerative features coexist since the earlier phases of the disease. During last years, attention has been directed toward the possible pathogenic pathways linking these two different features characterizing MS, in order to acquire a better understanding of the disease pathogenesis and to design new disease modifying therapies. Currently available therapies for MS are primarily aimed at modulating the immune system and are successfully used to reduce the risk of new inflammatory CNS lesions but show little or no efficacy in counteracting irreversible disease progression over time. Among the possible mechanism linking neuroinflamma-tion and neuronal loss, attention has been focused on the possible dysfunction of neuronal mitochondria during inflammatory CNS processes, since an impaired neuronal energetic support seems to represent a key event in the pathogenesis of neuro-axonal degener-ation.