help button home button Am J Pathol Angiogenesis Meeting
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Purchase Article
Right arrow View Shopping Cart
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Ahmed, Z.
Right arrow Articles by Cuzner, M. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Ahmed, Z.
Right arrow Articles by Cuzner, M. L.
(American Journal of Pathology. 2002;161:1577-1586.)
© 2002 American Society for Investigative Pathology

A Role for Caspase-1 and -3 in the Pathology of Experimental Allergic Encephalomyelitis

Inflammation Versus Degeneration

Zubair Ahmed*, Anne I. Doward*, Gareth Pryce*, Deanna L. Taylor*, Jennifer M. Pocock*, John P. Leonard{dagger}, David Baker* and M. Louise Cuzner*

From the Department of Neuroinflammation,* Institute of Neurology, University College London, London, United Kingdom; and Wyeth Research,{dagger} Andover, Massachusetts

Axonal loss, already present in the acute and first relapse phases of experimental allergic encephalomyelitis (EAE) in the ABH mouse, only becomes apparent in the third relapse in the interleukin-12 model of relapsing EAE in the Lewis rat. Caspase-1 immunostaining in the spinal cord of Lewis rats was mainly localized to inflammatory cuffs with the greatest proportion of active caspase-1-positive cells detected during the first and second relapses, correlating with enzyme activity and protein on Western blots. However, in the spinal cord of ABH mice during acute EAE, caspase-1 immunostaining was localized both on inflammatory and neuronal cells, again correlating with enzyme activity and protein production. In contrast, caspase-3 expression in the spinal cord of Lewis rats did not increase significantly until the third relapse when inflammatory and neuronal cells and axons became positive in line with a significant increase in caspase activity. In ABH mice active caspase-3 was already immunolocalized on axons and apoptotic neurons in the spinal cord during the acute stage of EAE. Because caspase-3 is a downstream cell death signal it may be possible to reduce apoptosis by selectively blocking caspase-3 and therefore provide a therapeutic target for EAE and potentially, multiple sclerosis.




This article has been cited by other articles:


Home page
 BrainHome page
P. G. Bannerman, A. Hahn, S. Ramirez, M. Morley, C. Bonnemann, S. Yu, G.-X. Zhang, A. Rostami, and D. Pleasure
Motor neuron pathology in experimental autoimmune encephalomyelitis: studies in THY1-YFP transgenic mice
Brain, August 1, 2005; 128(8): 1877 - 1886.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
M. Fernandez, A. Giuliani, S. Pirondi, G. D'Intino, L. Giardino, L. Aloe, R. Levi-Montalcini, and L. Calza
Thyroid hormone administration enhances remyelination in chronic demyelinating inflammatory disease
PNAS, November 16, 2004; 101(46): 16363 - 16368.
[Abstract] [Full Text] [PDF]

Home page
 BrainHome page
G. Pryce, Z. Ahmed, D. J. R. Hankey, S. J. Jackson, J. L. Croxford, J. M. Pocock, C. Ledent, A. Petzold, A. J. Thompson, G. Giovannoni, et al.
Cannabinoids inhibit neurodegeneration in models of multiple sclerosis
Brain, October 1, 2003; 126(10): 2191 - 2202.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 2002 by the American Society for Investigative Pathology.