Abstract:
:Aberrant activation of calpain plays a key role in the pathophysiology of several neurodegenerative disorders. Calpain is increasingly expressed in inflammatory cells in EAE and is significantly elevated in the white matter of patients with multiple sclerosis, thus calpain inhibition could be a target for therapeutic intervention. The experiments reported here employed a myelin oligodendrocyte glycoprotein-induced disease model in C57Bl/6 mice (EAE) and a novel calpain inhibitor, targeted to nervous tissue. CYLA was found to reduce clinical signs of EAE and prevent demyelination and inflammatory infiltration in a dose- and time-dependent manner. Oral administration of the diacetal prodrug was equally effective.
journal_name
J Neuroimmunoljournal_title
Journal of neuroimmunologyauthors
Hassen GW,Feliberti J,Kesner L,Stracher A,Mokhtarian Fdoi
10.1016/j.jneuroim.2006.08.005subject
Has Abstractpub_date
2006-11-01 00:00:00pages
135-46issue
1-2eissn
0165-5728issn
1872-8421pii
S0165-5728(06)00316-Xjournal_volume
180pub_type
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journal_title:Journal of neuroimmunology
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journal_title:Journal of neuroimmunology
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