Research articleIntrathecal insulin-like growth factor 1 but not insulin enhances myelin repair in young and aged rats

- Insulin-like growth factor 1 (IGF-1) enhanced remyelination in young and aged rats.
- Insulin, functionally related to IGF-1, did not enhance remyelination.
- Aged rats show less pronounced myelin repair compared to young rats.
- Aged rats are model for chronic demyelination faced in chronic multiple sclerosis.

One main pathological hallmark of multiple sclerosis (MS) is demyelination. Novel therapies which enhance myelin repair are urgently needed. Insulin and insulin-like growth factor 1 (IGF-1) have strong functional relationships. Here, we addressed the potential capacity of IGF-1 and insulin to enhance remyelination in an animal demyelination model in vivo. We found that chronic intrathecal infusion of IGF-1 enhanced remyelination after lysolecithin-induced demyelination in the spinal cord of young and aged rats. Aged rats showed a weaker innate remyelination capacity and are therefore a good model for progressive MS which is defined by chronic demyelination. In contrast to IGF-1, Insulin had no effect on remyelination in either age group. Our findings highlight the potential use of IGF-1 as remyelinating therapy for MS, particularly the progressive stage in which chronic demyelination is the hallmark.