Oxidative and nitrosative damage in multiple sclerosis

It is increasingly recognized that reactive oxygen and nitrogen species (ROS and RNS) are not only damaging molecules, but also essential signaling molecules regulating functions on organellar, cellular, organ, and organism levels. Nevertheless, damaging capacity of different ROS and RNS are connected to almost all diseases, including (neuro-)inflammation. One of the most frequent neuroinflammatory diseases is multiple sclerosis (MS). In this opinion article, we discuss recent advances in knowledge about oxidative and nitrosative damage, redox regulation, and the related ferroptotic cell death mechanism in initiation and progression of MS.

Specific improvement of supportive or inhibition of harmful redox processes in either brain or immune cells showed great impact on disease severity in MS models. Moreover, (circulating) markers of oxidative damage may hold promise as a supplementary diagnostic tool to differentiate different subtypes of MS.

Oxidative damage is well established as driver of MS. Nevertheless, molecular redox mechanisms underlying initiation and progression of MS are not well known. This existing research gaps impedes the establishment of successful antioxidative therapies.