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The Journal of Neuroscience, November 25, 2009, 29(47):14965-14979; doi:10.1523/JNEUROSCI.3794-09.2009

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Neurobiology of Disease
Initiation and Progression of Axonopathy in Experimental Autoimmune Encephalomyelitis

Athena M. Soulika, ^* Eunyoung Lee, ^* Erica McCauley, ^* Laird Miers, Peter Bannerman, and David Pleasure

Institute for Pediatric Regenerative Medicine, University of California Davis School of Medicine, Sacramento, California 95817

Correspondence should be addressed to Dr. David Pleasure, University of California Davis School of Medicine, c/o Shriners Hospital, 2425 Stockton Boulevard, Sacramento CA 95817. Email: david.pleasure{at}ucdmc.ucdavis.edu

Axonal loss is the principal cause of chronic disability in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE). In C57BL/6 mice with EAE induced by immunization with myelin oligodendrocyte glycoprotein peptide 35–55, the first evidences of axonal damage in spinal cord were in acute subpial and perivascular foci of infiltrating neutrophils and lymphocytes and included intra-axonal accumulations of the endovesicular Toll-like receptor TLR8, and the inflammasome protein NAcht leucine-rich repeat protein 1 (NALP1). Later in the course of this illness, focal inflammatory infiltrates disappeared from the spinal cord, but there was persistent activation of spinal cord innate immunity and progressive, bilaterally symmetric loss of small-diameter corticospinal tract axons. These results support the hypothesis that both contact-dependent and paracrine interactions of systemic inflammatory cells with axons and an innate immune-mediated neurodegenerative process contribute to axonal loss in this multiple sclerosis model.

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Received Aug. 4, 2009; revised Oct. 13, 2009; accepted Oct. 21, 2009.

Correspondence should be addressed to Dr. David Pleasure, University of California Davis School of Medicine, c/o Shriners Hospital, 2425 Stockton Boulevard, Sacramento CA 95817. Email: david.pleasure{at}ucdmc.ucdavis.edu

This article has been cited by other articles:

				F. Guo, Y. Maeda, J. Ma, J. Xu, M. Horiuchi, L. Miers, F. Vaccarino, and D. Pleasure Pyramidal Neurons Are Generated from Oligodendroglial Progenitor Cells in Adult Piriform Cortex J. Neurosci., September 8, 2010; 30(36): 12036 - 12049. [Abstract] [Full Text] [PDF]

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