Innovations In Clinical Neuroscience

HOTTOP Multiple Sclerosis DEC 2017

A peer-reviewed, evidence-based journal for clinicians in the field of neuroscience

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R E V I E W 22 Hot Topics in Multiple Sclerosis [December 2017] Neurol. 2014;262(Pt A):2–7. 54. Albanese M, Zagaglia S, Landi D, et al. Cerebrospinal fluid lactate is associated with multiple sclerosis disease progression. J Neuroinflammation. 2016;13(1):36. 55. Lutz NW, Viola A, Malikova I, et al. Inflammatory multiple-sclerosis plaques generate characteristic metabolic profiles in cerebrospinal fluid. PLoS One. 2007;2(7):e595. 56. Ciccarelli O, Toosy AT, De Stefano N, et al. Assessing neuronal metabolism in vivo by modeling imaging measures. J Neurosci. 2010;30(45):15030–3. 57. Stankiewicz JM, Neema M, Ceccarelli A. Iron and multiple sclerosis. Neurobiol Aging. 2014;35(Suppl 2):S51–8. 58. Hametner S, Wimmer I, Haider L, et al. Iron and neurodegeneration in the multiple sclerosis brain. Ann Neurol. 2013;74(6):848–61. 59. Neema M, Arora A, Healy BC, et al. Deep gray matter involvement on brain MRI scans is associated with clinical progression in multiple sclerosis. J Neuroimaging. 2009;19(1):3–8. 60. Ceccarelli A, Filippi M, Neema M, et al. T2 hypointensity in the deep gray matter of patients with benign multiple sclerosis. Mult Scler. 2009;15(6):678–86. 61. Worthington V, Killestein J, Eikelenboom MJ, et al. Normal CSF ferritin levels in MS suggest against etiologic role of chronic venous insufficiency. Neurology. 2010;75(18):1617–22. 62. Stadelmann C, Wegner C, Bruck W. Inflammation, demyelination, and degeneration—recent insights from MS pathology. Biochim Biophys Acta. 2011;1812(2):275–82. 63. Wekerle H. Lessons from multiple sclerosis: models, concepts, observations. Ann Rheum Dis. 2008;67(Suppl 3):iii56–60. 64. Kuhlmann T, Lingfeld G, Bitsch A, et al. Acute axonal damage in multiple sclerosis is most extensive in early disease stages and decreases over time. Brain. 2002;125(Pt 10):2202–12. 65. Magliozzi R, Howell OW, Reeves C, et al. A gradient of neuronal loss and meningeal inflammation in multiple sclerosis. Ann Neurol. 2010;68(4):477– 93. 66. Henderson AP, Barnett MH, Parratt JD, Prineas JW. Multiple sclerosis: distribution of inflammatory cells in newly forming lesions. Ann Neurol. 2009;66(6):739–53. 67. Hemmer B, Kerschensteiner M, Korn T. Role of the innate and adaptive immune responses in the course of multiple sclerosis. Lancet Neurol. 2015;14(4):406–19. 68. Steinman L, Zamvil SS. Beginning of the end of two-stage theory purporting that inflammation then degeneration explains pathogenesis of progressive multiple sclerosis. Curr Opin Neurol. 2016;29(3):340–4. 69. Cazzato G, Mesiano T, Antonello R, et al. Double-blind, placebo- controlled, randomized, crossover trial of high-dose methylprednisolone in patients with chronic progressive form of multiple sclerosis. Eur Neurol. 1995;35(4):193–8. 70. Wolinsky JS, Narayana PA, O'Connor P, et al. Glatiramer acetate in primary progressive multiple sclerosis: results of a multinational, multicenter, double-blind, placebo-controlled trial. Ann Neurol. 2007;61(1):14–24. 71. Hawker K, O'Connor P, Freedman MS, et al. Rituximab in patients with primary progressive multiple sclerosis: results of a randomized double-blind placebo-controlled multicenter trial. Ann Neurol. 2009;66(4):460–71. 72. Leary SM, Miller DH, Stevenson VL, et al. Interferon beta-1A in primary progressive MS: an exploratory, randomized, controlled trial. Neurology. 2003;60(1):44–51. 73. Montalban X, Sastre-Garriga J, Tintore M, et al. A single-center, randomized, double-blind, placebo-controlled study of interferon beta-1b on primary progressive and transitional multiple sclerosis. Mult Scler. 2009;15(10):1195–205. 74. Lublin F, Miller DH, Freedman MS, et al. Oral fingolimod in primary progressive multiple sclerosis (INFORMS): a phase 3, randomised, double-blind, placebo-controlled trial. Lancet. 2016;387(10023):1075–84. 75. Ziemssen T, Rauer S, Stadelmann, et al. Evaluation of study and patient characteristics of clinical studies in primary progressive multiple sclerosis: a systematic review. PLoS One. 2015;10(9):e0138243. 76. A Phase 2 Clinical Study in Subjects With Primary Progressive Multiple Sclerosis to Assess the Efficacy, Safety and Tolerability of Two Oral Doses of Laquinimod Either of 0.6 mg/Day or 1.5 mg/Day (Experimental Drug) as Compared to Placebo. 2017. 77. Dorner T, Burmester GR. New approaches of B-cell-directed therapy: beyond rituximab. Curr Opin Rheumatol. 2008;20(3):263–8. 78. Clynes RA, Towers TL, Presta LG, Ravetch JV. Inhibitory Fc receptors modulate in vivo cytotoxicity against tumor targets. Nat Med. 2000;6(4):443–6. 79. Roche. Roche's ocrelizumab first investigational medicine to show positive pivotal study results in both relapsing and primary progressive forms of multiple sclerosis. 2015. Available from: http://www.roche. com/media/store/releases/med- cor-2015-10-08.htm 80. Sedel F, Papeix C, Bellanger A, et al. High doses of biotin in chronic progressive multiple sclerosis: a pilot study. Mult Scler Relat Disord. 2015;4(2):159–69. 81. Thone J, Linker RA. Laquinimod in the treatment of multiple sclerosis: a review of the data so far. Drug Des Devel Ther. 2016;10:1111–8. 82. Jolivel V, Luessi F, Masri J, et al. Modulation of dendritic cell properties by laquinimod as a mechanism for modulating multiple sclerosis. Brain. 2013;136(Pt 4):1048–66. 83. Thone J, Ellrichmann G, Seubert S, et al. Modulation of autoimmune demyelination by laquinimod via induction of brain-derived neurotrophic factor. Am J Pathol. 2012;180(1):267–74.

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