Format

Send to

Choose Destination
J Neurosci. 2009 Nov 25;29(47):14965-79. doi: 10.1523/JNEUROSCI.3794-09.2009.

Initiation and progression of axonopathy in experimental autoimmune encephalomyelitis.

Author information

1
Institute for Pediatric Regenerative Medicine, University of California Davis School of Medicine, Sacramento, California 95817, USA.

Abstract

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.

PMID:
19940192
PMCID:
PMC2990681
DOI:
10.1523/JNEUROSCI.3794-09.2009
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for HighWire Icon for PubMed Central
Loading ...
Support Center