Are electrophysiological and oligodendrocyte alterations an element in the development of multiple sclerosis at the same time as or before the immune response?

References

• Ortiz GG, Pacheco-Moisés FP, Macías-Islas MA, et al. Role of the blood-brain barrier in multiple sclerosis. Arch Med Res. 2014;45(8):687–697.
   PubMed Web of Science ®Google Scholar
• Noseworthy JH, Lucchinetti C, Rodriguez M, et al. Multiple sclerosis. N Engl J Med. 2000;343(13):938–952.
   PubMed Web of Science ®Google Scholar
• Bitsch A, Schuchardt J, Bunkowski S, et al. Acute axonal injury in multiple sclerosis: correlation with demyelination and inflammation. Brain. 2000;123(6):1174–1183.
   PubMedGoogle Scholar
• Flores-Alvarado LJ, Ortiz GG, Pacheco-Moisés FP, et al. Mecanismos patogénicos en el Desarrollo de la esclerosis múltiple: ambiente, genes, sistema immune y estrés oxidatívo. Invest Clin. 2015;56(2):1–14.
   PubMedGoogle Scholar
• De Vos KJ, Grierson AJ, Ackerley S, et al. Role of axonal transport in neurodegenerative diseases. Annu Rev Neurosci. 2008;31:151–173.
   PubMed Web of Science ®Google Scholar
• Trapp BD, Nave KA. Multiple sclerosis: an immune or neurodegenerative disorder? Annu Rev Neurosci. 2008;31:247–269.
   PubMed Web of Science ®Google Scholar
• Brück W. The pathology of multiple sclerosis is the result of focal inflammatory demyelination with axonal damage. J Neurol. 2005;252(S5):v3–9.
   PubMedGoogle Scholar
• Soto-Brambila AP, Ortiz GG, Rivero-Moragrega P, et al. Relapsing remitting multiple sclerosis and its relationship with the immunology system and oxidative stress. Curr Immun Rev. 2018;14: 15–23.
   Google Scholar
• Ferguson B, Matyszak MK, Esiri MM, et al. Axonal damage in acute multiple sclerosis lesions. Brain. 1997;120(3):393–399.
   PubMedGoogle Scholar
• Bolton C, Paul C. Glutamate receptors in neuro-inflammatory demyelinating disease. Mediators Inflamm. 2006;2006:93684.
   PubMed Web of Science ®Google Scholar
• Saxena S, Caroni P. Mechanisms of axon degeneration: from development to disease. Prog Neurobiol. 2007;83(3):174–191.
   PubMed Web of Science ®Google Scholar
• Raine CS, Cross AH. Axonal dystrophy as a consequence of long-term demyelination. Lab Invest. 1989;60(5):714–725.
   PubMed Web of Science ®Google Scholar
• Irvine KA, Blakemore WF. Age increases axon loss associated with primary demyelination in cuprizone-induced demyelination in C57BL/6 mice. J Neuroimmunol. 2006;175(1–2):69–76.
   PubMed Web of Science ®Google Scholar
• Irvine KA, Blakemore WF. Remyelination protects axons from demyelination-associated axon degeneration. Brain. 2008;131(Pt 6):1464–1477.
   PubMedGoogle Scholar
• Brink BP, Veerhuis R, Breij EC, et al. The pathology of multiple sclerosis is location-dependent: no significant complement activation is detected in purely cortical lesions. J Neuropathol Exp Neurol. 2005;64(2):147–155.
   PubMed Web of Science ®Google Scholar
• Thompson AJ, Kermode AG, Wicks D, et al. Major differences in the dynamics of primary and secondary progressive multiple sclerosis. Ann Neurol. 1991;29(1):53–62.
   PubMed Web of Science ®Google Scholar
• 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):2202–2212.
   PubMedGoogle Scholar
• Frischer JM, Bramow S, Dal-Bianco A, et al. The relation between inflammation and neurodegeneration in multiple sclerosis brains. Brain. 2009;132(Pt 5):1175–1189.
   PubMed Web of Science ®Google Scholar
• Siebert H, Bruck W. The role of cytokines and adhesion molecules in axon degeneration after peripheral nerve axotomy: a study in different knockout mice. Brain Res. 2003;960(1–2):152–156.
   PubMed Web of Science ®Google Scholar
• Kornek B, Storch MK, Weissert R, et al. Multiple sclerosis and chronic autoimmune encephalomyelitis: a comparative quantitative study of axonal injury in active, inactive, and remyelinated lesions. Am J Pathol. 2000;157(1):267–276.
   PubMed Web of Science ®Google Scholar
• Bø L, Vedeler CA, Nyland H, et al. Intracortical multiple sclerosis lesions are not associated with increased lymphocyte infiltration. Mult Scler. 2003;9(4):323–331.
   PubMed Web of Science ®Google Scholar
• Nicot A, Ratnakar PV, Ron Y, et al. Regulation of gene expression in experimental autoimmune encephalomyelitis indicates early neuronal dysfunction. Brain. 2003;126(Pt 2):398–412.
   PubMedGoogle Scholar
• Kornek B, Lassmann H. Axonal pathology in multiple sclerosis. A historical note. Brain Pathol. 1999;9(4):651–656.
   PubMed Web of Science ®Google Scholar
• Williamson TL, Cleveland DW. Slowing of axonal transport is a very early event in the toxicity of ALS-linked SOD1 mutants to motor neurons. Nat Neurosci. 1999;2(1):50–56.
   PubMed Web of Science ®Google Scholar
• Koo EH, Sisodia SS, Archer DR, et al. Precursor of amyloid protein in Alzheimer disease undergoes fast anterograde axonal transport. Proc Natl Acad Sci USA. 1990;87(4):1561–1565.
   PubMed Web of Science ®Google Scholar
• Terwel D, Dewachter I, Van Leuven F. Axonal transport, tau protein, and neurodegeneration in Alzheimer’s disease. Neuromolecular Med. 2002;2(2):151–165.
   PubMed Web of Science ®Google Scholar
• Dziedzic T, Metz I, Dallenga T, et al. Wallerian degeneration: a major component of early axonal pathology in multiple sclerosis. Brain Pathol. 2010;20:976–985.
   PubMed Web of Science ®Google Scholar
• Filippi M, Cercignani M, Inglese M, et al. Diffusion tensor magnetic resonance imaging in multiple sclerosis. Neurology. 2001;56(3):304–311.
   PubMed Web of Science ®Google Scholar
• Arnold DL, Matthews PM, Francis G, et al. Proton magnetic resonance spectroscopy of human brain in vivo in the evaluation of multiple sclerosis: assessment of the load of disease. Magn Reson Med. 1990;14(1):154–159.
   PubMed Web of Science ®Google Scholar
• Wolinsky JS, Narayana PA, Fenstermacher MJ. Proton magnetic resonance spectroscopy in multiple sclerosis. Neurology. 1990;40(11):1764–1769.
   PubMed Web of Science ®Google Scholar
• Lassmann H. Pathogenic mechanisms associated with different clinical courses of multiple sclerosis. Front Immunol. 2018;9:3116.
   PubMed Web of Science ®Google Scholar
• Miller DH, Barkhof F, Frank JA, et al. Measurement of atrophy in multiple sclerosis: pathological basis, methodological aspects and clinical relevance. Brain. 2002;125(Pt 8):1676–1695.
   PubMed Web of Science ®Google Scholar
• Nielsen AS, Kinkel RP, Madigan N, et al. Contribution of cortical lesion subtypes at 7T MRI to physical and cognitive performance in MS. Neurology. 2013;81(7):641–649.
   PubMed Web of Science ®Google Scholar
• Androdias G, Reynolds R, Chanal M, et al. Meningeal T cells associate with diffuse axonal loss in multiple sclerosis spinal cords. Ann Neurol. 2010;68(4):465–476.
   PubMed Web of Science ®Google Scholar
• Haines JD, Inglese M, Casaccia P. Axonal damage in multiple sclerosis. Mt Sinai J Med. 2011;78(2):231–243.
   PubMedGoogle Scholar
• Inglese M, Madelin G, Oesingmann N, et al. Brain tissue sodium concentration in multiple sclerosis: a sodium imaging study at 3 tesla. Brain. 2010;133(3):847–857.
   PubMedGoogle Scholar
• Waxman SG. Axonal conduction and injury in multiple sclerosis: the role of sodium channels. Nat Rev Neurosci. 2006;7(12):932–941.
   PubMed Web of Science ®Google Scholar
• Smith KJ. Demyelinated and remyelinated axons, and their relation to symptom production in demyelinating disorders. Eye. 1994;8(2):224–237.
   PubMedGoogle Scholar
• Sá MJ. Physiopathology of symptoms and signs in multiple sclerosis. Arq Neuro-Psiquiatr. 2012;70(9):733–740.
   PubMed Web of Science ®Google Scholar
• Guo Z, Feng Z, Wang Y, et al. Simulation study of intermittent axonal block and desynchronization effect induced by high-frequency stimulation of electrical pulses. Front Neurosci. 2018;12:858.
   PubMed Web of Science ®Google Scholar
• Howe JF, Calvin WH, Loeser JD. Impulses reflected from dorsal root ganglia and from focal nerve injuries. Brain Res. 1976;116(1):139–144.
   PubMed Web of Science ®Google Scholar
• Amir R, Marshal D. Extra spike formation in sensory neurons and the disruption of afferent spike patterning. Biophys J. 2003;84(4):2700–2708.
   PubMed Web of Science ®Google Scholar
• Khare S, Seth D. Lhermitte's sign: the current status. Ann Indian Acad Neurol. 2015;18(2):154–156.
   PubMed Web of Science ®Google Scholar
• Rovaris M, Iannucci G, Falautano M, et al. Cognitive dysfunction in patients with mildly disabling relapsing-remitting multiple sclerosis: an exploratory study with diffusion tensor MR imaging. J Neurol Sci. 2002;195(2):103–109.
   PubMed Web of Science ®Google Scholar
• Trapp BD, Peterson J, Ransohoff RM, et al. Axonal transection in the lesions of multiple sclerosis. N Engl J Med. 1998;338(5):278–285.
   PubMed Web of Science ®Google Scholar
• Merril JE, Scolding NJ. Mechanisms of damage to myelin and oligodendrocytes and their relevance to disease. Neuropathol Appl Neurobiol. 1999;25(6):435–458.
   PubMed Web of Science ®Google Scholar
• Brück W. Inflammatory demyelination is not central to the pathogenesis of multiple sclerosis. J Neurol. 2005;252(S5):v10–15.
   PubMedGoogle Scholar
• Mahad DH, Trapp BD, Lassmann H. Pathological mechanisms in progressive multiple sclerosis. Lancet Neurol. 2015;14(2):183–193.
   PubMed Web of Science ®Google Scholar
• Kutzelnigg A, Lassmann H. Pathology of multiple sclerosis and related inflammatory demyelinating diseases. Handb Clin Neurol. 2014;122:15–58.
   PubMedGoogle Scholar
• Wegner C, Esiri MM, Chance SA, et al. Neocortical neuronal, synaptic, and glial loss in multiple sclerosis. Neurology. 2006;67(6):960–967.
   PubMed Web of Science ®Google Scholar
• Schirmer L, Velmeshev D, Holmqvist S, et al. Neuronal vulnerability and multilineage diversity in multiple sclerosis. Nature. 2019;573(7772):75–82.
   PubMed Web of Science ®Google Scholar
• Jäkel S, Agirre E, Mendanha Falcão A, et al. Altered human oligodendrocyte heterogeneity in multiple sclerosis. Nature. 2019;566(7745):543–547.
   PubMed Web of Science ®Google Scholar
• Giazkoulidou A, Messinis L, Nasios G. Cognitive functions and social cognition in multiple sclerosis: An overview. Hell J Nucl Med. 2019;22:102–110.
   PubMed Web of Science ®Google Scholar
• 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):571–584.
   PubMedGoogle Scholar
• Kozin MS, Kulakova OG, Favorova OO. Involvement of mitochondria in neurodegeneration in multiple sclerosis. Biochemistry Mosc. 2018;83(7):813–830.
   PubMed Web of Science ®Google Scholar
• Peruzzotti-Jametti L, Pluchino S. Targeting mitochondrial metabolism in neuroinflammation: towards a therapy for progressive multiple sclerosis. Trends Mol Med. 2018;24(10):838–855.
   PubMed Web of Science ®Google Scholar
• Campbell G, Mahad DJ. Mitochondrial dysfunction and axon degeneration in progressive multiple sclerosis. FEBS Lett. 2018;592(7):1113–1121.
   PubMed Web of Science ®Google Scholar