| Literature DB >> 26207848 |
Ruth Martha Stassart1, Gunther Helms2, Enrique Garea-Rodríguez3,4, Stefan Nessler1, Liat Hayardeny5, Christiane Wegner1, Christina Schlumbohm4,6, Eberhard Fuchs4,6,7, Wolfgang Brück1.
Abstract
Multiple sclerosis (MS) is the most common cause for sustained disability in young adults, yet treatment options remain very limited. Although numerous therapeutic approaches have been effective in rodent models of experimental autoimmune encephalomyelitis (EAE), only few proved to be beneficial in patients with MS. Hence, there is a strong need for more predictive animal models. Within the past decade, EAE in the common marmoset evolved as a potent, alternative model for MS, with immunological and pathological features resembling more closely the human disease. However, an often very rapid and severe disease course hampers its implementation for systematic testing of new treatment strategies. We here developed a new focal model of EAE in the common marmoset, induced by myelin oligodendrocyte glycoprotein (MOG) immunization and stereotactic injections of proinflammatory cytokines. At the injection site of cytokines, confluent inflammatory demyelinating lesions developed that strongly resembled human MS lesions. In a proof-of-principle treatment study with the immunomodulatory compound laquinimod, we demonstrate that targeted EAE in marmosets provides a promising and valid tool for preclinical experimental treatment trials in MS research.Entities:
Keywords: common marmoset; demyelination; experimental autoimmune encephalomyelitis; immunomodulation; laquinimod; multiple sclerosis
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Year: 2015 PMID: 26207848 DOI: 10.1111/bpa.12292
Source DB: PubMed Journal: Brain Pathol ISSN: 1015-6305 Impact factor: 6.508