Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

INTRODUCTION: Antibodies against myelin oligodendrocyte glycoprotein (MOG-IgG) are present in some neuromyelitis optica patients who lack antibodies against aquaporin-4 (AQP4-IgG). The effects of neuromyelitis optica MOG-IgG in the central nervous system have not been investigated in vivo. We microinjected MOG-IgG, obtained from patients with neuromyelitis optica, into mouse brains and compared the results with AQP4-IgG. RESULTS: MOG-IgG caused myelin changes and altered the expression of axonal proteins that are essential for action potential firing, but did not produce inflammation, axonal loss, neuronal or astrocyte death. These changes were independent of complement and recovered within two weeks. By contrast, AQP4-IgG produced complement-mediated myelin loss, neuronal and astrocyte death with limited recovery at two weeks. CONCLUSIONS: These differences mirror the better outcomes for MOG-IgG compared with AQP4-IgG patients and raise the possibility that MOG-IgG contributes to pathology in some neuromyelitis optica patients.

Original publication

DOI

10.1186/2051-5960-2-35

Type

Journal article

Journal

Acta Neuropathol Commun

Publication Date

31/03/2014

Volume

2

Keywords

Animals, Aquaporin 4, Astrocytes, Brain Injuries, Cell Adhesion Molecules, Neuronal, Humans, Immunoglobulin G, Mice, Myelin Basic Protein, Myelin-Oligodendrocyte Glycoprotein, Nerve Tissue Proteins, Neuromyelitis Optica, Neurons, Sodium Channels, Time Factors