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Published in: CNS Drugs 3/2017

01-03-2017 | Leading Article

Nogo-A Antibodies for Progressive Multiple Sclerosis

Authors: Benjamin V. Ineichen, Patricia S. Plattner, Nicolas Good, Roland Martin, Michael Linnebank, Martin E. Schwab

Published in: CNS Drugs | Issue 3/2017

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Abstract

Most of the current therapies, as well as many of the clinical trials, for multiple sclerosis (MS) target the inflammatory autoimmune processes, but less than 20% of all clinical trials investigate potential therapies for the chronic progressive disease stage of MS. The latter is responsible for the steadily increasing disability in many patients, and there is an urgent need for novel therapies that protect nervous system tissue and enhance axonal growth and/or remyelination. As outlined in this review, solid pre-clinical data suggest neutralization of the neurite outgrowth inhibitor Nogo-A as a potential new way to achieve both axonal and myelin repair. Several phase I clinical studies with anti-Nogo-A antibodies have been conducted in different disease paradigms including MS and spinal cord injury. Data from spinal cord injury and amyotrophic lateral sclerosis (ALS) trials accredit a good safety profile of high doses of anti-Nogo-A antibodies administered intravenously or intrathecally. An antibody against a Nogo receptor subunit, leucine rich repeat and immunoglobulin-like domain-containing protein 1 (LINGO-1), was recently shown to improve outcome in patients with acute optic neuritis in a phase II study. Nogo-A-suppressing antibodies could be novel drug candidates for the relapsing as well as the progressive MS disease stage. In this review, we summarize the available pre-clinical and clinical evidence on Nogo-A and elucidate the potential of Nogo-A-antibodies as a therapy for progressive MS.
Literature
1.
go back to reference World Health Organization. Multiple Sclerosis International Federation. Atlas: Multiple Sclerosis Resources in the World 2008. Geneva: World Health Organization; 2008. p. 13–7. World Health Organization. Multiple Sclerosis International Federation. Atlas: Multiple Sclerosis Resources in the World 2008. Geneva: World Health Organization; 2008. p. 13–7.
2.
go back to reference Trapp BD, Nave KA. Multiple sclerosis: an immune or neurodegenerative disorder? Annu Rev Neurosci. 2008;31:247–69.PubMedCrossRef Trapp BD, Nave KA. Multiple sclerosis: an immune or neurodegenerative disorder? Annu Rev Neurosci. 2008;31:247–69.PubMedCrossRef
3.
go back to reference Sawcer S, Hellenthal G, Pirinen M, et al. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature. 2011;476(7359):214–9.PubMedPubMedCentralCrossRef Sawcer S, Hellenthal G, Pirinen M, et al. Genetic risk and a primary role for cell-mediated immune mechanisms in multiple sclerosis. Nature. 2011;476(7359):214–9.PubMedPubMedCentralCrossRef
4.
go back to reference Tallantyre EC, Bo L, Al-Rawashdeh O, et al. Greater loss of axons in primary progressive multiple sclerosis plaques compared to secondary progressive disease. Brain. 2009;132(Pt 5):1190–9.PubMedCrossRef Tallantyre EC, Bo L, Al-Rawashdeh O, et al. Greater loss of axons in primary progressive multiple sclerosis plaques compared to secondary progressive disease. Brain. 2009;132(Pt 5):1190–9.PubMedCrossRef
5.
go back to reference Fox RJ, Thompson A, Baker D, et al. Setting a research agenda for progressive multiple sclerosis: the International Collaborative on Progressive MS. Mult Scler (Houndmills, Basingstoke, England). 2012;18(11):1534–40.CrossRef Fox RJ, Thompson A, Baker D, et al. Setting a research agenda for progressive multiple sclerosis: the International Collaborative on Progressive MS. Mult Scler (Houndmills, Basingstoke, England). 2012;18(11):1534–40.CrossRef
6.
go back to reference Torkildsen O, Myhr KM, Bo L. Disease-modifying treatments for multiple sclerosis: a review of approved medications. Eur J Neurol. 2016;23(Suppl. 1):18–27.PubMedCrossRef Torkildsen O, Myhr KM, Bo L. Disease-modifying treatments for multiple sclerosis: a review of approved medications. Eur J Neurol. 2016;23(Suppl. 1):18–27.PubMedCrossRef
7.
go back to reference Coles AJ, Cox A, Le Page E, et al. The window of therapeutic opportunity in multiple sclerosis: evidence from monoclonal antibody therapy. J Neurol. 2006;253(1):98–108.PubMedCrossRef Coles AJ, Cox A, Le Page E, et al. The window of therapeutic opportunity in multiple sclerosis: evidence from monoclonal antibody therapy. J Neurol. 2006;253(1):98–108.PubMedCrossRef
8.
go back to reference Hauser SL, Chan JR, Oksenberg JR. Multiple sclerosis: prospects and promise. Ann Neurol. 2013;74(3):317–27.PubMedCrossRef Hauser SL, Chan JR, Oksenberg JR. Multiple sclerosis: prospects and promise. Ann Neurol. 2013;74(3):317–27.PubMedCrossRef
9.
go back to reference Kappos L, Polman C, Pozzilli C, et al. Final analysis of the European multicenter trial on IFNbeta-1b in secondary-progressive MS. Neurology. 2001;57(11):1969–75.PubMedCrossRef Kappos L, Polman C, Pozzilli C, et al. Final analysis of the European multicenter trial on IFNbeta-1b in secondary-progressive MS. Neurology. 2001;57(11):1969–75.PubMedCrossRef
10.
go back to reference Hartung HP, Gonsette R, Konig N, et al. Mitoxantrone in progressive multiple sclerosis: a placebo-controlled, double-blind, randomised, multicentre trial. Lancet. 2002;360(9350):2018–25.PubMedCrossRef Hartung HP, Gonsette R, Konig N, et al. Mitoxantrone in progressive multiple sclerosis: a placebo-controlled, double-blind, randomised, multicentre trial. Lancet. 2002;360(9350):2018–25.PubMedCrossRef
11.
go back to reference Kappos L, Wiendl H, Selmaj K, et al. Daclizumab HYP versus interferon beta-1a in relapsing multiple sclerosis. N Engl J Med. 2015;373(15):1418–28.PubMedCrossRef Kappos L, Wiendl H, Selmaj K, et al. Daclizumab HYP versus interferon beta-1a in relapsing multiple sclerosis. N Engl J Med. 2015;373(15):1418–28.PubMedCrossRef
12.
go back to reference Gold R, Giovannoni G, Selmaj K, et al. Daclizumab high-yield process in relapsing-remitting multiple sclerosis (SELECT): a randomised, double-blind, placebo-controlled trial. Lancet. 2013;381(9884):2167–75.PubMedCrossRef Gold R, Giovannoni G, Selmaj K, et al. Daclizumab high-yield process in relapsing-remitting multiple sclerosis (SELECT): a randomised, double-blind, placebo-controlled trial. Lancet. 2013;381(9884):2167–75.PubMedCrossRef
13.
go back to reference Montalban X, Hemmer B, Rammohan K, et al. Efficacy and safety of ocrelizumab in primary progressive multiple sclerosis: results of the phase III double-blind, placebo-controlled ORATORIO study (S49.001). Neurology. 2016;86(16 Suppl.):S49-001. Montalban X, Hemmer B, Rammohan K, et al. Efficacy and safety of ocrelizumab in primary progressive multiple sclerosis: results of the phase III double-blind, placebo-controlled ORATORIO study (S49.001). Neurology. 2016;86(16 Suppl.):S49-001.
14.
go back to reference Hauser S, Comi G, Hartung H-P, et al. Efficacy and safety of ocrelizumab in relapsing multiple sclerosis-results of the interferon-beta-1a-controlled, double-blind, phase III OPERA I and II studies. Mult Scler. 2015;61–2. Hauser S, Comi G, Hartung H-P, et al. Efficacy and safety of ocrelizumab in relapsing multiple sclerosis-results of the interferon-beta-1a-controlled, double-blind, phase III OPERA I and II studies. Mult Scler. 2015;61–2.
15.
go back to reference McGinley MP, Moss BP, Cohen JA. Safety of monoclonal antibodies for the treatment of multiple sclerosis. Exp Opin Drug Saf. 2017;16(1):89–100.CrossRef McGinley MP, Moss BP, Cohen JA. Safety of monoclonal antibodies for the treatment of multiple sclerosis. Exp Opin Drug Saf. 2017;16(1):89–100.CrossRef
16.
go back to reference Ontaneda D, Fox RJ, Chataway J. Clinical trials in progressive multiple sclerosis: lessons learned and future perspectives. Lancet Neurol. 2015;14(2):208–23.PubMedPubMedCentralCrossRef Ontaneda D, Fox RJ, Chataway J. Clinical trials in progressive multiple sclerosis: lessons learned and future perspectives. Lancet Neurol. 2015;14(2):208–23.PubMedPubMedCentralCrossRef
19.
go back to reference Shirani A, Okuda DT, Stuve O. Therapeutic advances and future prospects in progressive forms of multiple sclerosis. Neurotherapeutics. 2016;13(1):58–69.PubMedPubMedCentralCrossRef Shirani A, Okuda DT, Stuve O. Therapeutic advances and future prospects in progressive forms of multiple sclerosis. Neurotherapeutics. 2016;13(1):58–69.PubMedPubMedCentralCrossRef
20.
go back to reference Trapp BD, Peterson J, Ransohoff RM, et al. Axonal transection in the lesions of multiple sclerosis. N Engl J Med. 1998;338(5):278–85.PubMedCrossRef Trapp BD, Peterson J, Ransohoff RM, et al. Axonal transection in the lesions of multiple sclerosis. N Engl J Med. 1998;338(5):278–85.PubMedCrossRef
21.
go back to reference Stadelmann C. Multiple sclerosis as a neurodegenerative disease: pathology, mechanisms and therapeutic implications. Curr Opin Neurol. 2011;24(3):224–9.PubMedCrossRef Stadelmann C. Multiple sclerosis as a neurodegenerative disease: pathology, mechanisms and therapeutic implications. Curr Opin Neurol. 2011;24(3):224–9.PubMedCrossRef
22.
go back to reference Weinshenker BG. The natural history of multiple sclerosis: update 1998. Semin Neurol. 1998;18(3):301–7.PubMedCrossRef Weinshenker BG. The natural history of multiple sclerosis: update 1998. Semin Neurol. 1998;18(3):301–7.PubMedCrossRef
23.
go back to reference Filippi M, Rocca MA, De Stefano N, et al. Magnetic resonance techniques in multiple sclerosis: the present and the future. Arch Neurol. 2011;68(12):1514–20.PubMedCrossRef Filippi M, Rocca MA, De Stefano N, et al. Magnetic resonance techniques in multiple sclerosis: the present and the future. Arch Neurol. 2011;68(12):1514–20.PubMedCrossRef
24.
go back to reference Criste G, Trapp B, Dutta R. Axonal loss in multiple sclerosis: causes and mechanisms. Handb Clin Neurol. 2014;122:101–13.PubMedCrossRef Criste G, Trapp B, Dutta R. Axonal loss in multiple sclerosis: causes and mechanisms. Handb Clin Neurol. 2014;122:101–13.PubMedCrossRef
25.
go back to reference Mahad DH, Trapp BD, Lassmann H. Pathological mechanisms in progressive multiple sclerosis. Lancet Neurol. 2015;14(2):183–93.PubMedCrossRef Mahad DH, Trapp BD, Lassmann H. Pathological mechanisms in progressive multiple sclerosis. Lancet Neurol. 2015;14(2):183–93.PubMedCrossRef
26.
go back to reference Fischer MT, Sharma R, Lim JL, et al. NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury. Brain. 2012;135(Pt 3):886–99.PubMedPubMedCentralCrossRef Fischer MT, Sharma R, Lim JL, et al. NADPH oxidase expression in active multiple sclerosis lesions in relation to oxidative tissue damage and mitochondrial injury. Brain. 2012;135(Pt 3):886–99.PubMedPubMedCentralCrossRef
27.
go back to reference Campbell GR, Kraytsberg Y, Krishnan KJ, et al. Clonally expanded mitochondrial DNA deletions within the choroid plexus in multiple sclerosis. Acta Neuropathol. 2012;124(2):209–20.PubMedPubMedCentralCrossRef Campbell GR, Kraytsberg Y, Krishnan KJ, et al. Clonally expanded mitochondrial DNA deletions within the choroid plexus in multiple sclerosis. Acta Neuropathol. 2012;124(2):209–20.PubMedPubMedCentralCrossRef
28.
go back to reference Witte ME, Mahad DJ, Lassmann H, van Horssen J. Mitochondrial dysfunction contributes to neurodegeneration in multiple sclerosis. Trends Mol Med. 2014;20(3):179–87.PubMedCrossRef Witte ME, Mahad DJ, Lassmann H, van Horssen J. Mitochondrial dysfunction contributes to neurodegeneration in multiple sclerosis. Trends Mol Med. 2014;20(3):179–87.PubMedCrossRef
29.
go back to reference Dendrou CA, Fugger L, Friese MA. Immunopathology of multiple sclerosis. Nat Rev Immunol. 2015;15(9):545–58.PubMedCrossRef Dendrou CA, Fugger L, Friese MA. Immunopathology of multiple sclerosis. Nat Rev Immunol. 2015;15(9):545–58.PubMedCrossRef
30.
go back to reference Sorbara CD, Wagner NE, Ladwig A, et al. Pervasive axonal transport deficits in multiple sclerosis models. Neuron. 2014;84(6):1183–90.PubMedCrossRef Sorbara CD, Wagner NE, Ladwig A, et al. Pervasive axonal transport deficits in multiple sclerosis models. Neuron. 2014;84(6):1183–90.PubMedCrossRef
31.
go back to reference Davies AL, Desai RA, Bloomfield PS, et al. Neurological deficits caused by tissue hypoxia in neuroinflammatory disease. Ann Neurol. 2013;74(6):815–25.PubMedCrossRef Davies AL, Desai RA, Bloomfield PS, et al. Neurological deficits caused by tissue hypoxia in neuroinflammatory disease. Ann Neurol. 2013;74(6):815–25.PubMedCrossRef
32.
33.
go back to reference Lassmann H. Demyelination and neurodegeneration in multiple sclerosis: the role of hypoxia. Ann Neurol. 2016;79(4):520–1.PubMedCrossRef Lassmann H. Demyelination and neurodegeneration in multiple sclerosis: the role of hypoxia. Ann Neurol. 2016;79(4):520–1.PubMedCrossRef
34.
go back to reference Patani R, Balaratnam M, Vora A, Reynolds R. Remyelination can be extensive in multiple sclerosis despite a long disease course. Neuropathol Appl Neurobiol. 2007;33(3):277–87.PubMedCrossRef Patani R, Balaratnam M, Vora A, Reynolds R. Remyelination can be extensive in multiple sclerosis despite a long disease course. Neuropathol Appl Neurobiol. 2007;33(3):277–87.PubMedCrossRef
35.
go back to reference Franklin RJ, Gallo V. The translational biology of remyelination: past, present, and future. Glia. 2014;62(11):1905–15.PubMedCrossRef Franklin RJ, Gallo V. The translational biology of remyelination: past, present, and future. Glia. 2014;62(11):1905–15.PubMedCrossRef
36.
37.
go back to reference Franklin RJ, Ffrench-Constant C, Edgar JM, Smith KJ. Neuroprotection and repair in multiple sclerosis. Nat Rev Neurol. 2012;8(11):624–34.PubMedCrossRef Franklin RJ, Ffrench-Constant C, Edgar JM, Smith KJ. Neuroprotection and repair in multiple sclerosis. Nat Rev Neurol. 2012;8(11):624–34.PubMedCrossRef
38.
go back to reference Craner MJ, Newcombe J, Black JA, et al. Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger. Proc Natl Acad Sci USA. 2004;101(21):8168–73.PubMedPubMedCentralCrossRef Craner MJ, Newcombe J, Black JA, et al. Molecular changes in neurons in multiple sclerosis: altered axonal expression of Nav1.2 and Nav1.6 sodium channels and Na+/Ca2+ exchanger. Proc Natl Acad Sci USA. 2004;101(21):8168–73.PubMedPubMedCentralCrossRef
39.
go back to reference Vergo S, Craner MJ, Etzensperger R, et al. Acid-sensing ion channel 1 is involved in both axonal injury and demyelination in multiple sclerosis and its animal model. Brain. 2011;134(Pt 2):571–84.PubMedCrossRef Vergo S, Craner MJ, Etzensperger R, et al. Acid-sensing ion channel 1 is involved in both axonal injury and demyelination in multiple sclerosis and its animal model. Brain. 2011;134(Pt 2):571–84.PubMedCrossRef
40.
go back to reference Friese MA, Craner MJ, Etzensperger R, et al. Acid-sensing ion channel-1 contributes to axonal degeneration in autoimmune inflammation of the central nervous system. Nat Med. 2007;13(12):1483–9.PubMedCrossRef Friese MA, Craner MJ, Etzensperger R, et al. Acid-sensing ion channel-1 contributes to axonal degeneration in autoimmune inflammation of the central nervous system. Nat Med. 2007;13(12):1483–9.PubMedCrossRef
41.
go back to reference Schattling B, Steinbach K, Thies E, et al. TRPM4 cation channel mediates axonal and neuronal degeneration in experimental autoimmune encephalomyelitis and multiple sclerosis. Nat Med. 2012;18(12):1805–11.PubMedCrossRef Schattling B, Steinbach K, Thies E, et al. TRPM4 cation channel mediates axonal and neuronal degeneration in experimental autoimmune encephalomyelitis and multiple sclerosis. Nat Med. 2012;18(12):1805–11.PubMedCrossRef
42.
go back to reference Friese MA, Schattling B, Fugger L. Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis. Nat Rev Neurol. 2014;10(4):225–38.PubMedCrossRef Friese MA, Schattling B, Fugger L. Mechanisms of neurodegeneration and axonal dysfunction in multiple sclerosis. Nat Rev Neurol. 2014;10(4):225–38.PubMedCrossRef
43.
go back to reference Frischer JM, Weigand SD, Guo Y, et al. Clinical and pathological insights into the dynamic nature of the white matter multiple sclerosis plaque. Ann Neurol. 2015;78(5):710–21.PubMedPubMedCentralCrossRef Frischer JM, Weigand SD, Guo Y, et al. Clinical and pathological insights into the dynamic nature of the white matter multiple sclerosis plaque. Ann Neurol. 2015;78(5):710–21.PubMedPubMedCentralCrossRef
44.
go back to reference Mews I, Bergmann M, Bunkowski S, et al. Oligodendrocyte and axon pathology in clinically silent multiple sclerosis lesions. Mult Scler. 1998;4(2):55–62.PubMedCrossRef Mews I, Bergmann M, Bunkowski S, et al. Oligodendrocyte and axon pathology in clinically silent multiple sclerosis lesions. Mult Scler. 1998;4(2):55–62.PubMedCrossRef
45.
go back to reference Bjartmar C, Kidd G, Mork S, et al. Neurological disability correlates with spinal cord axonal loss and reduced N-acetyl aspartate in chronic multiple sclerosis patients. Ann Neurol. 2000;48(6):893–901.PubMedCrossRef Bjartmar C, Kidd G, Mork S, et al. Neurological disability correlates with spinal cord axonal loss and reduced N-acetyl aspartate in chronic multiple sclerosis patients. Ann Neurol. 2000;48(6):893–901.PubMedCrossRef
46.
go back to reference Sospedra M, Martin R. Immunology of multiple sclerosis. Ann Rev Immunol. 2005;23:683–747.CrossRef Sospedra M, Martin R. Immunology of multiple sclerosis. Ann Rev Immunol. 2005;23:683–747.CrossRef
47.
go back to reference Dubois-Dalcq M, Ffrench-Constant C, Franklin RJ. Enhancing central nervous system remyelination in multiple sclerosis. Neuron. 2005;48(1):9–12.PubMedCrossRef Dubois-Dalcq M, Ffrench-Constant C, Franklin RJ. Enhancing central nervous system remyelination in multiple sclerosis. Neuron. 2005;48(1):9–12.PubMedCrossRef
48.
go back to reference Wootla B, Denic A, Watzlawik JO, et al. Antibody-mediated oligodendrocyte remyelination promotes axon health in progressive demyelinating disease. Mol Neurobiol. 2016;53(8):5217–28.PubMedCrossRef Wootla B, Denic A, Watzlawik JO, et al. Antibody-mediated oligodendrocyte remyelination promotes axon health in progressive demyelinating disease. Mol Neurobiol. 2016;53(8):5217–28.PubMedCrossRef
49.
go back to reference Schwab ME. Functions of Nogo proteins and their receptors in the nervous system. Nat Rev Neurosci. 2010;11(12):799–811.PubMedCrossRef Schwab ME. Functions of Nogo proteins and their receptors in the nervous system. Nat Rev Neurosci. 2010;11(12):799–811.PubMedCrossRef
50.
go back to reference Caroni P, Schwab ME. Antibody against myelin-associated inhibitor of neurite growth neutralizes nonpermissive substrate properties of CNS white matter. Neuron. 1988;1(1):85–96.PubMedCrossRef Caroni P, Schwab ME. Antibody against myelin-associated inhibitor of neurite growth neutralizes nonpermissive substrate properties of CNS white matter. Neuron. 1988;1(1):85–96.PubMedCrossRef
51.
go back to reference GrandPre T, Nakamura F, Vartanian T, Strittmatter SM. Identification of the Nogo inhibitor of axon regeneration as a reticulon protein. Nature. 2000;403(6768):439–44.PubMedCrossRef GrandPre T, Nakamura F, Vartanian T, Strittmatter SM. Identification of the Nogo inhibitor of axon regeneration as a reticulon protein. Nature. 2000;403(6768):439–44.PubMedCrossRef
52.
go back to reference Chen MS, Huber AB, van der Haar ME, et al. Nogo-A is a myelin-associated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1. Nature. 2000;403(6768):434–9.PubMedCrossRef Chen MS, Huber AB, van der Haar ME, et al. Nogo-A is a myelin-associated neurite outgrowth inhibitor and an antigen for monoclonal antibody IN-1. Nature. 2000;403(6768):434–9.PubMedCrossRef
53.
go back to reference Schwab ME, Strittmatter SM. Nogo limits neural plasticity and recovery from injury. Curr Opin Neurobiol. 2014;27:53–60.PubMedCrossRef Schwab ME, Strittmatter SM. Nogo limits neural plasticity and recovery from injury. Curr Opin Neurobiol. 2014;27:53–60.PubMedCrossRef
54.
go back to reference Huber AB, Weinmann O, Brosamle C, et al. Patterns of Nogo mRNA and protein expression in the developing and adult rat and after CNS lesions. J Neurosci. 2002;22(9):3553–67.PubMed Huber AB, Weinmann O, Brosamle C, et al. Patterns of Nogo mRNA and protein expression in the developing and adult rat and after CNS lesions. J Neurosci. 2002;22(9):3553–67.PubMed
55.
go back to reference Dodd DA, Niederoest B, Bloechlinger S, et al. Nogo-A, -B, and -C are found on the cell surface and interact together in many different cell types. J Biol Chem. 2005;280(13):12494–502.PubMedCrossRef Dodd DA, Niederoest B, Bloechlinger S, et al. Nogo-A, -B, and -C are found on the cell surface and interact together in many different cell types. J Biol Chem. 2005;280(13):12494–502.PubMedCrossRef
56.
go back to reference Wang KC, Koprivica V, Kim JA, et al. Oligodendrocyte-myelin glycoprotein is a Nogo receptor ligand that inhibits neurite outgrowth. Nature. 2002;417(6892):941–4.PubMedCrossRef Wang KC, Koprivica V, Kim JA, et al. Oligodendrocyte-myelin glycoprotein is a Nogo receptor ligand that inhibits neurite outgrowth. Nature. 2002;417(6892):941–4.PubMedCrossRef
57.
go back to reference Nash M, Pribiag H, Fournier AE, Jacobson C. Central nervous system regeneration inhibitors and their intracellular substrates. Mol Neurobiol. 2009;40(3):224–35.PubMedCrossRef Nash M, Pribiag H, Fournier AE, Jacobson C. Central nervous system regeneration inhibitors and their intracellular substrates. Mol Neurobiol. 2009;40(3):224–35.PubMedCrossRef
58.
go back to reference Kempf A, Tews B, Arzt ME, et al. The sphingolipid receptor S1PR2 is a receptor for Nogo-a repressing synaptic plasticity. PLoS Biol. 2014;12(1):e1001763.PubMedPubMedCentralCrossRef Kempf A, Tews B, Arzt ME, et al. The sphingolipid receptor S1PR2 is a receptor for Nogo-a repressing synaptic plasticity. PLoS Biol. 2014;12(1):e1001763.PubMedPubMedCentralCrossRef
59.
go back to reference Montani L, Gerrits B, Gehrig P, et al. Neuronal Nogo-A modulates growth cone motility via Rho-GTP/LIMK1/cofilin in the unlesioned adult nervous system. J Biol Chem. 2009;284(16):10793–807.PubMedPubMedCentralCrossRef Montani L, Gerrits B, Gehrig P, et al. Neuronal Nogo-A modulates growth cone motility via Rho-GTP/LIMK1/cofilin in the unlesioned adult nervous system. J Biol Chem. 2009;284(16):10793–807.PubMedPubMedCentralCrossRef
60.
go back to reference Gou X, Zhang Q, Xu N, et al. Spatio-temporal expression of paired immunoglobulin-like receptor-B in the adult mouse brain after focal cerebral ischaemia. Brain Inj. 2013;27(11):1311–5.PubMedCrossRef Gou X, Zhang Q, Xu N, et al. Spatio-temporal expression of paired immunoglobulin-like receptor-B in the adult mouse brain after focal cerebral ischaemia. Brain Inj. 2013;27(11):1311–5.PubMedCrossRef
61.
go back to reference Mi S, Pepinsky RB, Cadavid D. Blocking LINGO-1 as a therapy to promote CNS repair: from concept to the clinic. CNS Drugs. 2013;27(7):493–503.PubMedCrossRef Mi S, Pepinsky RB, Cadavid D. Blocking LINGO-1 as a therapy to promote CNS repair: from concept to the clinic. CNS Drugs. 2013;27(7):493–503.PubMedCrossRef
62.
go back to reference Barrette B, Vallieres N, Dube M, Lacroix S. Expression profile of receptors for myelin-associated inhibitors of axonal regeneration in the intact and injured mouse central nervous system. Mol Cell Neurosci. 2007;34(4):519–38.PubMedCrossRef Barrette B, Vallieres N, Dube M, Lacroix S. Expression profile of receptors for myelin-associated inhibitors of axonal regeneration in the intact and injured mouse central nervous system. Mol Cell Neurosci. 2007;34(4):519–38.PubMedCrossRef
63.
go back to reference Fujita Y, Yamashita T. Axon growth inhibition by RhoA/ROCK in the central nervous system. Frontiers Neurosci. 2014;8:338.CrossRef Fujita Y, Yamashita T. Axon growth inhibition by RhoA/ROCK in the central nervous system. Frontiers Neurosci. 2014;8:338.CrossRef
64.
go back to reference Teng FY, Tang BL. Why do Nogo/Nogo-66 receptor gene knockouts result in inferior regeneration compared to treatment with neutralizing agents? J Neurochem. 2005;94(4):865–74.PubMedCrossRef Teng FY, Tang BL. Why do Nogo/Nogo-66 receptor gene knockouts result in inferior regeneration compared to treatment with neutralizing agents? J Neurochem. 2005;94(4):865–74.PubMedCrossRef
65.
go back to reference Lee JK, Geoffroy CG, Chan AF, et al. Assessing spinal axon regeneration and sprouting in Nogo-, MAG-, and OMgp-deficient mice. Neuron. 2010;66(5):663–70.PubMedPubMedCentralCrossRef Lee JK, Geoffroy CG, Chan AF, et al. Assessing spinal axon regeneration and sprouting in Nogo-, MAG-, and OMgp-deficient mice. Neuron. 2010;66(5):663–70.PubMedPubMedCentralCrossRef
66.
go back to reference Schmandke A, Schmandke A, Schwab ME. Nogo-A: multiple roles in CNS development, maintenance, and disease. Neuroscientist. 2014;20(4):372–86.PubMedCrossRef Schmandke A, Schmandke A, Schwab ME. Nogo-A: multiple roles in CNS development, maintenance, and disease. Neuroscientist. 2014;20(4):372–86.PubMedCrossRef
67.
go back to reference Chong SY, Rosenberg SS, Fancy SP, et al. Neurite outgrowth inhibitor Nogo-A establishes spatial segregation and extent of oligodendrocyte myelination. Proc Natl Acad Sci USA. 2012;109(4):1299–304.PubMedCrossRef Chong SY, Rosenberg SS, Fancy SP, et al. Neurite outgrowth inhibitor Nogo-A establishes spatial segregation and extent of oligodendrocyte myelination. Proc Natl Acad Sci USA. 2012;109(4):1299–304.PubMedCrossRef
68.
go back to reference Gonzenbach RR, Zoerner B, Schnell L, et al. Delayed anti-nogo-a antibody application after spinal cord injury shows progressive loss of responsiveness. J Neurotrauma. 2012;29(3):567–78.PubMedCrossRef Gonzenbach RR, Zoerner B, Schnell L, et al. Delayed anti-nogo-a antibody application after spinal cord injury shows progressive loss of responsiveness. J Neurotrauma. 2012;29(3):567–78.PubMedCrossRef
69.
70.
go back to reference Tsai SY, Papadopoulos CM, Schwab ME, Kartje GL. Delayed anti-nogo-a therapy improves function after chronic stroke in adult rats. Stroke. 2011;42(1):186–90.PubMedCrossRef Tsai SY, Papadopoulos CM, Schwab ME, Kartje GL. Delayed anti-nogo-a therapy improves function after chronic stroke in adult rats. Stroke. 2011;42(1):186–90.PubMedCrossRef
71.
go back to reference Markus TM, Tsai SY, Bollnow MR, et al. Recovery and brain reorganization after stroke in adult and aged rats. Ann Neurol. 2005;58(6):950–3.PubMedCrossRef Markus TM, Tsai SY, Bollnow MR, et al. Recovery and brain reorganization after stroke in adult and aged rats. Ann Neurol. 2005;58(6):950–3.PubMedCrossRef
72.
go back to reference Wahl AS, Omlor W, Rubio JC, et al. Neuronal repair. Asynchronous therapy restores motor control by rewiring of the rat corticospinal tract after stroke. Science (New York, NY). 2014;344(6189):1250–5.CrossRef Wahl AS, Omlor W, Rubio JC, et al. Neuronal repair. Asynchronous therapy restores motor control by rewiring of the rat corticospinal tract after stroke. Science (New York, NY). 2014;344(6189):1250–5.CrossRef
73.
go back to reference Freund P, Schmidlin E, Wannier T, et al. Nogo-A-specific antibody treatment enhances sprouting and functional recovery after cervical lesion in adult primates. Nat Med. 2006;12(7):790–2.PubMedCrossRef Freund P, Schmidlin E, Wannier T, et al. Nogo-A-specific antibody treatment enhances sprouting and functional recovery after cervical lesion in adult primates. Nat Med. 2006;12(7):790–2.PubMedCrossRef
74.
go back to reference Zagrebelsky M, Schweigreiter R, Bandtlow CE, et al. Nogo-A stabilizes the architecture of hippocampal neurons. J Neurosci. 2010;30(40):13220–34.PubMedCrossRef Zagrebelsky M, Schweigreiter R, Bandtlow CE, et al. Nogo-A stabilizes the architecture of hippocampal neurons. J Neurosci. 2010;30(40):13220–34.PubMedCrossRef
75.
go back to reference Delekate A, Zagrebelsky M, Kramer S, et al. NogoA restricts synaptic plasticity in the adult hippocampus on a fast time scale. Proc Natl Acad Sci. 2011;108(6):2569–74.PubMedPubMedCentralCrossRef Delekate A, Zagrebelsky M, Kramer S, et al. NogoA restricts synaptic plasticity in the adult hippocampus on a fast time scale. Proc Natl Acad Sci. 2011;108(6):2569–74.PubMedPubMedCentralCrossRef
76.
77.
go back to reference Zemmar A, Weinmann O, Kellner Y, et al. Neutralization of Nogo-A enhances synaptic plasticity in the rodent motor cortex and improves motor learning in vivo. J Neurosci. 2014;34(26):8685–98.PubMedPubMedCentralCrossRef Zemmar A, Weinmann O, Kellner Y, et al. Neutralization of Nogo-A enhances synaptic plasticity in the rodent motor cortex and improves motor learning in vivo. J Neurosci. 2014;34(26):8685–98.PubMedPubMedCentralCrossRef
78.
go back to reference Wills ZP, Mandel-Brehm C, Mardinly AR, et al. The nogo receptor family restricts synapse number in the developing hippocampus. Neuron. 2012;73(3):466–81.PubMedPubMedCentralCrossRef Wills ZP, Mandel-Brehm C, Mardinly AR, et al. The nogo receptor family restricts synapse number in the developing hippocampus. Neuron. 2012;73(3):466–81.PubMedPubMedCentralCrossRef
79.
go back to reference Lee JY, Petratos S. Multiple sclerosis: does Nogo play a role? Neuroscientist. 2013;19(4):394–408.PubMedCrossRef Lee JY, Petratos S. Multiple sclerosis: does Nogo play a role? Neuroscientist. 2013;19(4):394–408.PubMedCrossRef
80.
go back to reference Karnezis T, Mandemakers W, McQualter JL, et al. The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination. Nat Neurosci. 2004;7(7):736–44.PubMedCrossRef Karnezis T, Mandemakers W, McQualter JL, et al. The neurite outgrowth inhibitor Nogo A is involved in autoimmune-mediated demyelination. Nat Neurosci. 2004;7(7):736–44.PubMedCrossRef
81.
go back to reference Fontoura P, Ho PP, DeVoss J, et al. Immunity to the extracellular domain of Nogo-A modulates experimental autoimmune encephalomyelitis. J Immunol. 2004;173(11):6981–92.PubMedCrossRef Fontoura P, Ho PP, DeVoss J, et al. Immunity to the extracellular domain of Nogo-A modulates experimental autoimmune encephalomyelitis. J Immunol. 2004;173(11):6981–92.PubMedCrossRef
82.
go back to reference Fontoura P, Steinman L. Nogo in multiple sclerosis: growing roles of a growth inhibitor. Journal of the neurological sciences. J Neurol Sci. 2006;245(1–2):201–10.PubMedCrossRef Fontoura P, Steinman L. Nogo in multiple sclerosis: growing roles of a growth inhibitor. Journal of the neurological sciences. J Neurol Sci. 2006;245(1–2):201–10.PubMedCrossRef
83.
go back to reference Petratos S, Ozturk E, Azari MF, et al. Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation. Brain. 2012;135(Pt 6):1794–818.PubMedPubMedCentralCrossRef Petratos S, Ozturk E, Azari MF, et al. Limiting multiple sclerosis related axonopathy by blocking Nogo receptor and CRMP-2 phosphorylation. Brain. 2012;135(Pt 6):1794–818.PubMedPubMedCentralCrossRef
85.
go back to reference Nikic I, Merkler D, Sorbara C, et al. A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis. Nat Med. 2011;17(4):495–9.PubMedCrossRef Nikic I, Merkler D, Sorbara C, et al. A reversible form of axon damage in experimental autoimmune encephalomyelitis and multiple sclerosis. Nat Med. 2011;17(4):495–9.PubMedCrossRef
86.
go back to reference Tomassini V, d’Ambrosio A, Petsas N, et al. The effect of inflammation and its reduction on brain plasticity in multiple sclerosis: MRI evidence. Hum Brain Mapp. 2016;37(7):2431–45.PubMedPubMedCentralCrossRef Tomassini V, d’Ambrosio A, Petsas N, et al. The effect of inflammation and its reduction on brain plasticity in multiple sclerosis: MRI evidence. Hum Brain Mapp. 2016;37(7):2431–45.PubMedPubMedCentralCrossRef
87.
go back to reference Bareyre FM, Kerschensteiner M, Raineteau O, et al. The injured spinal cord spontaneously forms a new intraspinal circuit in adult rats. Nat Neurosci. 2004;7(3):269–77.PubMedCrossRef Bareyre FM, Kerschensteiner M, Raineteau O, et al. The injured spinal cord spontaneously forms a new intraspinal circuit in adult rats. Nat Neurosci. 2004;7(3):269–77.PubMedCrossRef
88.
go back to reference Kerschensteiner M, Bareyre FM, Buddeberg BS, et al. Remodeling of axonal connections contributes to recovery in an animal model of multiple sclerosis. J Exp Med. 2004;200(8):1027–38.PubMedPubMedCentralCrossRef Kerschensteiner M, Bareyre FM, Buddeberg BS, et al. Remodeling of axonal connections contributes to recovery in an animal model of multiple sclerosis. J Exp Med. 2004;200(8):1027–38.PubMedPubMedCentralCrossRef
89.
go back to reference Theotokis P, Lourbopoulos A, Touloumi O, et al. Time course and spatial profile of Nogo-A expression in experimental autoimmune encephalomyelitis in C57BL/6 mice. J Neuropathol Exp Neurol. 2012;71(10):907–20.PubMedCrossRef Theotokis P, Lourbopoulos A, Touloumi O, et al. Time course and spatial profile of Nogo-A expression in experimental autoimmune encephalomyelitis in C57BL/6 mice. J Neuropathol Exp Neurol. 2012;71(10):907–20.PubMedCrossRef
90.
go back to reference Anderson JM, Hampton DW, Patani R, et al. Abnormally phosphorylated tau is associated with neuronal and axonal loss in experimental autoimmune encephalomyelitis and multiple sclerosis. Brain. 2008;131(Pt 7):1736–48.PubMedCrossRef Anderson JM, Hampton DW, Patani R, et al. Abnormally phosphorylated tau is associated with neuronal and axonal loss in experimental autoimmune encephalomyelitis and multiple sclerosis. Brain. 2008;131(Pt 7):1736–48.PubMedCrossRef
91.
go back to reference Denic A, Johnson AJ, Bieber AJ, et al. The relevance of animal models in multiple sclerosis research. Pathophysiology. 2011;18(1):21–9.PubMedCrossRef Denic A, Johnson AJ, Bieber AJ, et al. The relevance of animal models in multiple sclerosis research. Pathophysiology. 2011;18(1):21–9.PubMedCrossRef
92.
go back to reference Jaillard C, Harrison S, Stankoff B, et al. Edg8/S1P5: an oligodendroglial receptor with dual function on process retraction and cell survival. J Neurosci. 2005;25(6):1459–69.PubMedCrossRef Jaillard C, Harrison S, Stankoff B, et al. Edg8/S1P5: an oligodendroglial receptor with dual function on process retraction and cell survival. J Neurosci. 2005;25(6):1459–69.PubMedCrossRef
93.
go back to reference Pernet V, Joly S, Christ F, et al. Nogo-A and myelin-associated glycoprotein differently regulate oligodendrocyte maturation and myelin formation. J Neurosci. 2008;28(29):7435–44.PubMedCrossRef Pernet V, Joly S, Christ F, et al. Nogo-A and myelin-associated glycoprotein differently regulate oligodendrocyte maturation and myelin formation. J Neurosci. 2008;28(29):7435–44.PubMedCrossRef
94.
go back to reference Syed YA, Baer AS, Lubec G, et al. Inhibition of oligodendrocyte precursor cell differentiation by myelin-associated proteins. Neurosurg Focus. 2008;24(3–4):E5.PubMedCrossRef Syed YA, Baer AS, Lubec G, et al. Inhibition of oligodendrocyte precursor cell differentiation by myelin-associated proteins. Neurosurg Focus. 2008;24(3–4):E5.PubMedCrossRef
95.
go back to reference Mi S, Miller RH, Lee X, et al. LINGO-1 negatively regulates myelination by oligodendrocytes. Nat Neurosci. 2005;8(6):745–51.PubMedCrossRef Mi S, Miller RH, Lee X, et al. LINGO-1 negatively regulates myelination by oligodendrocytes. Nat Neurosci. 2005;8(6):745–51.PubMedCrossRef
96.
go back to reference Mi S, Hu B, Hahm K, et al. LINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis. Nat Med. 2007;13(10):1228–33.PubMedCrossRef Mi S, Hu B, Hahm K, et al. LINGO-1 antagonist promotes spinal cord remyelination and axonal integrity in MOG-induced experimental autoimmune encephalomyelitis. Nat Med. 2007;13(10):1228–33.PubMedCrossRef
97.
go back to reference Mi S, Miller RH, Tang W, et al. Promotion of central nervous system remyelination by induced differentiation of oligodendrocyte precursor cells. Ann Neurol. 2009;65(3):304–15.PubMedCrossRef Mi S, Miller RH, Tang W, et al. Promotion of central nervous system remyelination by induced differentiation of oligodendrocyte precursor cells. Ann Neurol. 2009;65(3):304–15.PubMedCrossRef
98.
go back to reference Lee X, Yang Z, Shao Z, et al. NGF regulates the expression of axonal LINGO-1 to inhibit oligodendrocyte differentiation and myelination. J Neurosci. 2007;27(1):220–5.PubMedCrossRef Lee X, Yang Z, Shao Z, et al. NGF regulates the expression of axonal LINGO-1 to inhibit oligodendrocyte differentiation and myelination. J Neurosci. 2007;27(1):220–5.PubMedCrossRef
99.
go back to reference Wootla B, Watzlawik JO, Warrington AE, et al. Naturally occurring monoclonal antibodies and their therapeutic potential for neurologic diseases. JAMA Neurol. 2015;72(11):1346–53.PubMedCrossRef Wootla B, Watzlawik JO, Warrington AE, et al. Naturally occurring monoclonal antibodies and their therapeutic potential for neurologic diseases. JAMA Neurol. 2015;72(11):1346–53.PubMedCrossRef
100.
go back to reference Satoh J, Onoue H, Arima K, Yamamura T. Nogo-A and nogo receptor expression in demyelinating lesions of multiple sclerosis. J Neuropathol Exp Neurol. 2005;64(2):129–38.PubMedCrossRef Satoh J, Onoue H, Arima K, Yamamura T. Nogo-A and nogo receptor expression in demyelinating lesions of multiple sclerosis. J Neuropathol Exp Neurol. 2005;64(2):129–38.PubMedCrossRef
101.
go back to reference Reindl M, Khantane S, Ehling R, et al. Serum and cerebrospinal fluid antibodies to Nogo-A in patients with multiple sclerosis and acute neurological disorders. J Neuroimmunol. 2003;145(1–2):139–47.PubMedCrossRef Reindl M, Khantane S, Ehling R, et al. Serum and cerebrospinal fluid antibodies to Nogo-A in patients with multiple sclerosis and acute neurological disorders. J Neuroimmunol. 2003;145(1–2):139–47.PubMedCrossRef
102.
go back to reference Meininger V, Pradat PF, Corse A, et al. Safety, pharmacokinetic, and functional effects of the nogo-a monoclonal antibody in amyotrophic lateral sclerosis: a randomized, first-in-human clinical trial. PLoS One. 2014;9(5):e97803.PubMedPubMedCentralCrossRef Meininger V, Pradat PF, Corse A, et al. Safety, pharmacokinetic, and functional effects of the nogo-a monoclonal antibody in amyotrophic lateral sclerosis: a randomized, first-in-human clinical trial. PLoS One. 2014;9(5):e97803.PubMedPubMedCentralCrossRef
103.
go back to reference Tran JQ, Rana J, Barkhof F, et al. Randomized phase I trials of the safety/tolerability of anti-LINGO-1 monoclonal antibody BIIB033. Neurol Neuroimmunol Neuroinflamm. 2014;1(2):e18.PubMedPubMedCentralCrossRef Tran JQ, Rana J, Barkhof F, et al. Randomized phase I trials of the safety/tolerability of anti-LINGO-1 monoclonal antibody BIIB033. Neurol Neuroimmunol Neuroinflamm. 2014;1(2):e18.PubMedPubMedCentralCrossRef
104.
go back to reference Cadavid D, Balcer L, Galetta S, et al. Evidence of remyelination with the anti-LINGO-1 monoclonal antibody BIIB033 after acute optic neuritis. Neurology. 2015; E46. Cadavid D, Balcer L, Galetta S, et al. Evidence of remyelination with the anti-LINGO-1 monoclonal antibody BIIB033 after acute optic neuritis. Neurology. 2015; E46.
105.
go back to reference Noseworthy JH, Vandervoort MK, Wong CJ, Ebers GC. Interrater variability with the Expanded Disability Status Scale (EDSS) and Functional Systems (FS) in a multiple sclerosis clinical trial: the Canadian Cooperation MS Study Group. Neurology. 1990;40(6):971–5.PubMedCrossRef Noseworthy JH, Vandervoort MK, Wong CJ, Ebers GC. Interrater variability with the Expanded Disability Status Scale (EDSS) and Functional Systems (FS) in a multiple sclerosis clinical trial: the Canadian Cooperation MS Study Group. Neurology. 1990;40(6):971–5.PubMedCrossRef
106.
go back to reference di Nuzzo L, Orlando R, Nasca C, Nicoletti F. Molecular pharmacodynamics of new oral drugs used in the treatment of multiple sclerosis. Drug Design Develop Ther. 2014;8:555–68. di Nuzzo L, Orlando R, Nasca C, Nicoletti F. Molecular pharmacodynamics of new oral drugs used in the treatment of multiple sclerosis. Drug Design Develop Ther. 2014;8:555–68.
107.
go back to reference Bonnan M, Ferrari S, Bertandeau E, et al. Intrathecal rituximab therapy in multiple sclerosis: review of evidence supporting the need for future trials. Curr Drug Targets. 2014;15(13):1205–14.PubMedCrossRef Bonnan M, Ferrari S, Bertandeau E, et al. Intrathecal rituximab therapy in multiple sclerosis: review of evidence supporting the need for future trials. Curr Drug Targets. 2014;15(13):1205–14.PubMedCrossRef
108.
go back to reference Bien-Ly N, Boswell CA, Jeet S, et al. Lack of widespread BBB disruption in Alzheimer’s disease models: focus on therapeutic antibodies. Neuron. 2015;88(2):289–97.PubMedCrossRef Bien-Ly N, Boswell CA, Jeet S, et al. Lack of widespread BBB disruption in Alzheimer’s disease models: focus on therapeutic antibodies. Neuron. 2015;88(2):289–97.PubMedCrossRef
109.
go back to reference Pepinsky RB, Shao Z, Ji B, et al. Exposure levels of anti-LINGO-1 Li81 antibody in the central nervous system and dose-efficacy relationships in rat spinal cord remyelination models after systemic administration. J Pharmacol Exp Ther. 2011;339(2):519–29.PubMedCrossRef Pepinsky RB, Shao Z, Ji B, et al. Exposure levels of anti-LINGO-1 Li81 antibody in the central nervous system and dose-efficacy relationships in rat spinal cord remyelination models after systemic administration. J Pharmacol Exp Ther. 2011;339(2):519–29.PubMedCrossRef
110.
go back to reference Petereit HF, Rubbert-Roth A. Rituximab levels in cerebrospinal fluid of patients with neurological autoimmune disorders. Mult Scler. 2009;15(2):189–92.PubMedCrossRef Petereit HF, Rubbert-Roth A. Rituximab levels in cerebrospinal fluid of patients with neurological autoimmune disorders. Mult Scler. 2009;15(2):189–92.PubMedCrossRef
111.
go back to reference Tran J, Palaparthy R, Zhao J, et al. Safety, tolerability and pharmacokinetics of the anti-LINGO-1 monoclonal antibody BIIB033 in healthy volunteers and subjects with multiple sclerosis. Neurology. 2012;78((Meeting Abstracts 1)):P02.021. Tran J, Palaparthy R, Zhao J, et al. Safety, tolerability and pharmacokinetics of the anti-LINGO-1 monoclonal antibody BIIB033 in healthy volunteers and subjects with multiple sclerosis. Neurology. 2012;78((Meeting Abstracts 1)):P02.021.
112.
go back to reference Greenberg BM, Rodriguez M, Kantarci O, et al. Safety and tolerability of the remyelinating therapeutic antibody rHIgM22 in patients with stable multiple sclerosis. Neurology. 2015:E48–E49. Greenberg BM, Rodriguez M, Kantarci O, et al. Safety and tolerability of the remyelinating therapeutic antibody rHIgM22 in patients with stable multiple sclerosis. Neurology. 2015:E48–E49.
113.
go back to reference Willi R, Schwab ME. Nogo and Nogo receptor: relevance to schizophrenia? Neurobiol Dis. 2013;54:150–7.PubMedCrossRef Willi R, Schwab ME. Nogo and Nogo receptor: relevance to schizophrenia? Neurobiol Dis. 2013;54:150–7.PubMedCrossRef
114.
go back to reference Lewis CM, Levinson DF, Wise LH, et al. Genome scan meta-analysis of schizophrenia and bipolar disorder, part II: schizophrenia. Am J Hum Genet. 2003;73(1):34–48.PubMedPubMedCentralCrossRef Lewis CM, Levinson DF, Wise LH, et al. Genome scan meta-analysis of schizophrenia and bipolar disorder, part II: schizophrenia. Am J Hum Genet. 2003;73(1):34–48.PubMedPubMedCentralCrossRef
115.
go back to reference Willi R, Weinmann O, Winter C, et al. Constitutive genetic deletion of the growth regulator Nogo-A induces schizophrenia-related endophenotypes. J Neurosci. 2010;30(2):556–67.PubMedCrossRef Willi R, Weinmann O, Winter C, et al. Constitutive genetic deletion of the growth regulator Nogo-A induces schizophrenia-related endophenotypes. J Neurosci. 2010;30(2):556–67.PubMedCrossRef
116.
go back to reference Budel S, Padukkavidana T, Liu BP, et al. Genetic variants of Nogo-66 receptor with possible association to schizophrenia block myelin inhibition of axon growth. J Neurosci. 2008;28(49):13161–72.PubMedPubMedCentralCrossRef Budel S, Padukkavidana T, Liu BP, et al. Genetic variants of Nogo-66 receptor with possible association to schizophrenia block myelin inhibition of axon growth. J Neurosci. 2008;28(49):13161–72.PubMedPubMedCentralCrossRef
117.
go back to reference Craveiro LM, Weinmann O, Roschitzki B, et al. Infusion of anti-Nogo-A antibodies in adult rats increases growth and synapse related proteins in the absence of behavioral alterations. Exp Neurol. 2013;250:52–68.PubMedCrossRef Craveiro LM, Weinmann O, Roschitzki B, et al. Infusion of anti-Nogo-A antibodies in adult rats increases growth and synapse related proteins in the absence of behavioral alterations. Exp Neurol. 2013;250:52–68.PubMedCrossRef
118.
go back to reference Oertle T, van der Haar ME, Bandtlow CE, et al. Nogo-A inhibits neurite outgrowth and cell spreading with three discrete regions. J Neurosci. 2003;23(13):5393–406.PubMed Oertle T, van der Haar ME, Bandtlow CE, et al. Nogo-A inhibits neurite outgrowth and cell spreading with three discrete regions. J Neurosci. 2003;23(13):5393–406.PubMed
119.
go back to reference Schnell L, Schwab ME. Axonal regeneration in the rat spinal cord produced by an antibody against myelin-associated neurite growth inhibitors. Nature. 1990;343(6255):269–72.PubMedCrossRef Schnell L, Schwab ME. Axonal regeneration in the rat spinal cord produced by an antibody against myelin-associated neurite growth inhibitors. Nature. 1990;343(6255):269–72.PubMedCrossRef
Metadata
Title
Nogo-A Antibodies for Progressive Multiple Sclerosis
Authors
Benjamin V. Ineichen
Patricia S. Plattner
Nicolas Good
Roland Martin
Michael Linnebank
Martin E. Schwab
Publication date
01-03-2017
Publisher
Springer International Publishing
Published in
CNS Drugs / Issue 3/2017
Print ISSN: 1172-7047
Electronic ISSN: 1179-1934
DOI
https://doi.org/10.1007/s40263-017-0407-2

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