Brain Advance Access published online on May 12, 2008
Brain, doi:10.1093/brain/awn076
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Review Article |
From fish to man: understanding endogenous remyelination in central nervous system demyelinating diseases
1National Institute for Neurological Disorders and Stroke (NINDS), Porter Neuroscience Center, National Institutes of Health, Bethesda, MD, 20892, USA, 2Department of Clinical Neurosciences, Western General Hospital, Edinburgh, UK, 3Institute of Neuropathology, University Medical Center, D-37075 Goettingen, Germany, 4Inserm, U711, 75013 Paris, 5Université Pierre & Marie Curie, Faculté de médecine, IFR 70 and 6AP-HP, Hôpital de la Salpêtrière, 75013 Paris, France
Correspondence to:
Monique Dubois-Dalcq, MD, National Institute of Neurological Disorders and Stroke, Porter Neuroscience Research Center, Bdg 35, Pod 2A106, 35 Convent Drive MSC3706, Bethesda MD 20892-3706, USA E-mail: mdalcq{at}pasteur.fr; dalcqm{at}mail.nih.gov
In the central nervous system (CNS) of man, evolutionary pressure has preserved some capability for remyelination while axonal regeneration is very limited. In contrast, two efficient programmes of regeneration exist in the adult fish CNS, neurite regrowth and remyelination. The rapidity of CNS remyelination is critical since it not only restores fast conduction of nerve impulses but also maintains axon integrity. If myelin repair fails, axons degenerate, leading to increased disability. In the human CNS demyelinating disease multiple sclerosis (MS), remyelination often takes place in the midst of inflammation. Here, we discuss recent studies that address the innate repair capabilities of the axon-glia unit from fish to man. We propose that expansion of this research field will help find ways to maintain or enhance spontaneous remyelination in man.
Key Words: multiple sclerosis; nodes of Ranvier; enhancing repair; animal models; transparent fish
Abbreviations: AMPA, amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid; BDNF, brain-derived neurotrophic factor; BMB, 1,4-bis (p-aminostyryl)-2-methoxy benzene); CNS, central nervous system; CNTF, ciliary neurotrophic factor; CXCL, alpha chemokines; CXCLR, alpha chemokine receptor; DTI, diffusion tensor imaging; EAE, experimental autoimmune encephalitis; EB, ethidium bromide; EGF, epidermal growth factor; FGF-R, fibroblast growth factor receptor; GAG, glycosaminoglycan; IFN, interferon; LIF, leukemia inhibitory factor; LtBr, lymphotoxin beta receptor; MRI, magnetic resonance imaging; MS, multiple sclerosis; MTR, magnetisation transfer ratio; Nfasc, neurofascin; NMDA, N-methyl-D-aspartate; Nrg 1, neuregulin 1; OPC, oligodendrocyte precursor cells; PDGF A, platelet-derived growth factor A; PDGF-R, PDGF receptor; PET, positron emission tomography; PNS, peripheral nervous system; PSA-NCAM, polysialylated neural adhesion molecule; Sema, semaphorin; SVZ, subventricular zone; TGFbeta, transforming growth factor beta
Received January 31, 2008. Revised March 18, 2008. Accepted March 26, 2008.