Special considerations for care taking of animals with EAE as well as potential applications and limitations of this model are discussed. Mice are evaluated daily using a clinical scoring system for 25-50 days. Mice develop a "classic" self-limited monophasic EAE with ascending flaccid paralysis within 9-14 days after immunization. The immunogenic epitope MOG35-55 is suspended in complete Freund's adjuvant (CFA) prior to immunization and pertussis toxin is applied on the day of immunization and two days later. C57BL/6 mice are the commonly used strain for transgenic mouse construction and respond among others to myelin oligodendrocyte glycoprotein (MOG). EAE susceptibility and phenotype depends on the chosen antigen and rodent strain. Due to the low immunogenic potential of these peptides, strong adjuvants are used. Therefore, mice are immunized with CNS homogenates or peptides of myelin proteins. It is especially suited for investigating the effects of drugs or of particular genes by using transgenic mice challenged by autoimmune neuroinflammation. Actively-induced EAE in mice is the easiest inducible model with robust and replicable results. There is a broad diversity of EAE models which reflect different clinical, immunological and histological aspects of human MS. Experimental autoimmune encephalomyelitis (EAE) is the most common animal model for MS sharing many clinical and pathophysiological features. MS therapy is only partially effective so far and research efforts continue to expand our knowledge on the pathophysiology of the disease and to develop novel treatment strategies. While the exact etiology of the disease is yet unclear, autoreactive T lymphocytes are thought to play a central role in its pathophysiology. Some acute plaques (I and II) may exhibit some remyelination, demonstrated by presence of thin myelin wraps and oligodendrocyte precursor cells recruited to the lesion epicenter 7, 23. Multiple sclerosis is a chronic neuroinflammatory demyelinating disorder of the central nervous system with a strong neurodegenerative component. Observation of these clinical signs should cue testing for autoantibodies, specifically aquaporin-4 and myelin oligodendrocyte glycoprotein.
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