Early axon damage in EAE

E
Recks MS, Stormanns ER, Bader J, Arnhold S, Addicks K, Kuerten S. Early axonal damage and progressive myelin pathology define the kinetics of CNS histopathology in a mouse model of multiple sclerosis. Clin Immunol. 2013 ;149(1):32-45. doi: 10.1016/j.clim.2013.06.004. [Epub ahead of print]


Studies of MS histopathology are largely dependent on suitable animal models. While light microscopic analysis gives an overview of tissue pathology, it falls short in evaluating detailed changes in nerve fibre morphology. The ultrastructural data presented here and obtained from studies of myelin oligodendrocyte glycoprotein (MOG):35-55-induced experimental autoimmune encephalomyelitis (EAE) in C57BL/6 mice delineate that axonal damage and myelin pathology follow different kinetics in the disease course. While myelin pathology accumulated with disease progression, axonal damage coincided with the initial clinical disease symptoms and remained stable over time. This pattern applied both to irreversible axolysis and early axonal pathology. Notably, these histopathological patterns were reflected by the normal-appearing white matter (NAWM), suggesting that the NAWM is also in an active neurodegenerative state. The data underline the need for neuroprotection in MS and suggest the MOG model as a highly valuable tool for the assessment of different therapeutic strategies.

Axonal loss occurs early and then remains stable…this is because disease in C57BL/6 is monphasic (it has one attack) and nerves are lost….Is this a good model of MS..yet it isbeing used increasily.

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MouseDoctor

2 comments

  • Does monophasic mean PPMS? Regarding neuroprotection: How could the axon be preserved if it loses the trophic support of the oligodendrocyte?

  • Soory this was posted before I had probably finished it but

    No monophasic means one attack.

    There are many that think this equates to PPMS..dubious I think. However I think it shows that progression can start after one attack because these beasts show progressive worsening, but probably not in the context of this study.

    In this report they are suggesting the axons goes before the melin. There are many ways to neurprotect

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