Abstract

Pediatric-onset multiple sclerosis (MS) represents an important unmet clinical need as well as a unique opportunity to study early disease mechanisms. While some features (including degree of focal–inflammatory activity, apparent recovery from acute relapse) differ between pediatric- and adult-onset MS, shared genetic and environmental risk factors across the age spectrum suggest that mechanisms underlying MS development in children are in essence the same as in adults, and that any differences may be more likely to reflect manifestation of the same disease in younger and still maturing immune and nervous systems. The shorter interval between biological and clinical onset in children with MS limits the number of irrelevant exposures or biological abnormalities that may emerge as a consequence (rather than cause) of disease. Here, we review genetic and environmental risk factors implicated in the pediatric MS population and summarize emerging insights into early humoral and cellular immune targets and mechanisms involved in disease pathogenesis.

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