We appreciate Altmann’s interest in our article.1 Our intention was certainly not to be provocative but rather to draw attention to scientific facts that negate the assumed immunopathogenesis of MS. He is confused regarding the context of the quotation from Bell and Lathrop.2 The quotation was cited to show the fallacy of experimental EAE as a putative model for MS, not for disease epidemiology. Like others, he displays the same blind faith that the association of HLA markers supports an autoimmune model of MS. There are genes within the HLA locus that have nothing to do with immune function; indeed, the strongest HLA associations are with hemochromatosis and narcolepsy, which have no immune basis and are examples of metabolic and neurodegenerative diseases. Similarly, while natalizumab is an effective therapy in reducing clinical relapses and enhancing lesions in the magnetic resonance imaging of patients with relapsing-remitting MS, its mechanism of action is probably limited to the permeability of the blood-brain barrier. There is no evidence as yet that natalizumab has any effect on the progressive disease that is primarily related to neurodegeneration. Prevention of relapses in MS may not translate into prevention of long-term disability.
Chaudhuri A, Behan PO. Evaluating the Evidence for Multiple Sclerosis as an Autoimmune Disease—Reply. Arch Neurol. 2005;62(4):688–689. doi:10.1001/archneur.62.4.688-b
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