Axonal damage in multiple sclerosis: a complex issue in a complex disease.
Multiple sclerosis is no longer considered to simply be an autoimmune demyelinating disease. Axonal destruction is another central pathological feature and a contributor to the accumulating disability of disease progression. The mechanism underlying axonal pathology has not been fully clarified but does not appear to be a simple one. The relationship between axonal damage and other components of the pathological features such as demyelination, inflammation and remyelination are under intense investigation. Experimental data suggest that therapeutic interventions such as the induction of rapid remyelination may lead to the protection of axons. In addition to immunomodulation, future strategies for neuroprotection may be of great importance.
Grigoriadis
Nikolaos
N
Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, 1 Stilp. Kyriakidi Str., 54636 Thessaloniki, Greece. grigoria@med.auth.gr
Ben-Hur
Tamir
T
Karussis
Dimitrios
D
Milonas
Ioannis
I
D000276:Adjuvants, Immunologic / Q000627:therapeutic use; D001369:Axons / Q000473:pathology*; D001921:Brain / Q000473:pathology*; D003711:Demyelinating Diseases / Q000473:pathology; D003937:Diagnosis, Differential; D018698:Glutamic Acid / Q000378:metabolism; D006801:Humans; D016899:Interferon-beta / Q000627:therapeutic use; D008264:Macrophages / Q000378:metabolism; D008279:Magnetic Resonance Imaging; D009103:Multiple Sclerosis / Q000188:drug therapy / Q000378:metabolism / Q000473:pathology*; D009186:Myelin Sheath / Q000473:pathology; D009410:Nerve Degeneration / Q000378:metabolism / Q000473:pathology
D000276:Adjuvants, Immunologic; D018698:Glutamic Acid; D016899:Interferon-beta