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

Neurosci Lett. 2017 May 1:648:41-46. doi: 10.1016/j.neulet.2017.03.047. Epub 2017 Mar 29.

Abstract

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.

Keywords: IGF-1; Insulin; Intrathecal; Lysolecithin; Multiple sclerosis; Rat; Remyelination.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Blood Glucose
  • Cell Count
  • Demyelinating Diseases / chemically induced
  • Demyelinating Diseases / prevention & control*
  • Female
  • Injections, Spinal
  • Insulin / administration & dosage*
  • Insulin-Like Growth Factor I / administration & dosage*
  • Lysophosphatidylcholines
  • Macrophages / drug effects
  • Macrophages / metabolism
  • Myelin Sheath / drug effects*
  • Rats
  • Rats, Long-Evans

Substances

  • Blood Glucose
  • Insulin
  • Lysophosphatidylcholines
  • Insulin-Like Growth Factor I