Ions, energy and axonal injury: towards a molecular neurology of multiple sclerosis.
It is now clear that effective treatments for nervous system disorders such as multiple sclerosis (MS) represent achievable objectives. Molecular mechanisms of axonal degeneration - a major pathological substrate for disability in MS - have been identified, pointing to the possibility of neuroprotection. Although previous studies were mainly carried out in laboratory models, recent analyses of human MS tissue have identified molecular targets that are related to mitochondrial function and specific isoforms of ion channels as contributors to axonal degeneration in MS. Taken together, the observations in model systems and in human tissue converge on the identification of a group of molecules that are related to ion fluxes and energetics as significant actors in the axonal-injury cascade, and suggest a set of molecular targets that might be useful in the development of new therapies.
Waxman
Stephen G
SG
Department of Neurology, LCI 707, Yale Medical School, P.O. Box 208018, New Haven, CT 06520, USA. stephen.waxman@yale.edu
D000818:Animals; D017920:Antiporters / Q000378:metabolism; D001369:Axons / Q000473:pathology*; D004195:Disease Models, Animal; D004734:Energy Metabolism; D006801:Humans; D007473:Ion Channels / Q000378:metabolism; D008967:Molecular Biology; D009103:Multiple Sclerosis / Q000378:metabolism* / Q000473:pathology*; D009462:Neurology
D017920:Antiporters; D007473:Ion Channels