Prospects of repair in multiple sclerosis

In multiple sclerosis, physiological repair mechanisms can help the nervous system to recover from tissue injury. Enhancing such repair mechanisms is an important, and increasingly realistic, therapeutic goal in multiple sclerosis. With respect to remyelination, several promising therapeutic avenues are currently being explored, including stem cell transplantation, LINGO-1, prolactin and glatiramer acetate. Glatiramer acetate is believed to act by the induction of specific populations of anti-inflammatory Th2 cells or Type 2 monocytes which infiltrate sites of injury in the nervous system where they release anti-inflammatory cytokines leading to bystander suppression of inflammation. In addition, these cells can release neurotrophic factors such as BDNF and IGF-1 which have been shown to stimulate the differentiation of oligodendrocyte precursor cells and thus enhance remyelination. In addition, neurotrophic factors released in response to glatiramer acetate may stimulate the differentiation of neuronal progenitor cells into mature neurones that can replace neurones lost through the disease process. This repair capacity of glatiramer acetate may contribute to the long-term well-being of patients with multiple sclerosis treated with glatiramer acetate.