Rogan wrote:Two problems with the standard model.
1. Hasn't found a root cause in 50 years.
2. The model's entire evidence base is off of inflicting healthy mice with EAE.
Mice are not humans and humans with "MS" don't get EAE.
SJL mice display a very high incidence of reticulum cell sarcomas resembling Hodgkin's disease by approximately one year of age. This strain is also characterized by extreme aggression in males and its susceptibility to experimental autoimmune encephalomyelitis (EAE) for multiple sclerosis research. SJL/J mice develop a spontaneous myopathy resulting from a splice-site mutation in the Dysferlin gene resulting in decreased levels of dysferlin protein in SJL/J mice and making this strain a good model for limb girdle muscular dystrophy 2B. SJL mice, fed an atherogenic diet (1.25% cholesterol, 0.5% cholic acid and 15% fat), fail to develop atherosclerotic aortic lesions in contrast to several highly susceptible strains of mice. SJL are immunocompetent but have elevated levels of circulating T cells.
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