Cookies on this website

We use cookies to ensure that we give you the best experience on our website. If you click 'Accept all cookies' we'll assume that you are happy to receive all cookies and you won't see this message again. If you click 'Reject all non-essential cookies' only necessary cookies providing core functionality such as security, network management, and accessibility will be enabled. Click 'Find out more' for information on how to change your cookie settings.

Damage to axons in acute multiple sclerosis (MS) lesions is now well established but the mechanisms of this damage remain obscure. Here we have applied a panel of antibodies that identify cell populations and proteins contained in them with a view to detecting those cells and proteins that are localised particularly closely to damaged axons in acute, sub-acute and border-active MS plaques. Results are expressed semi-quantitatively and graphs produced that show that many of the markers show enhanced expression at sites of axon damage. However, the sharpest increase in expression in relation to axon damage was seen for Calpain I (micro-calpain), inducible nitric oxide synthase and MMP-2, suggesting that these proteins may form part of a group of proteins responsible for the initiation of myelin and/or axon damage seen in MS lesions.

Original publication

DOI

10.1007/s00401-006-0045-0

Type

Journal article

Journal

Acta Neuropathol

Publication Date

04/2006

Volume

111

Pages

289 - 299

Keywords

Amyloid beta-Peptides, Antigens, CD, Antigens, Differentiation, Myelomonocytic, Axons, Biomarkers, Brain, CD3 Complex, Calpain, Humans, Immunohistochemistry, Matrix Metalloproteinase 2, Matrix Metalloproteinase 9, Multiple Sclerosis, Nitric Oxide Synthase Type II, Osteopontin, Plaque, Amyloid, Proteins, Sialoglycoproteins, T-Lymphocytes, Tyrosine