Abstract
Multiple Sclerosis (MS) is shown to have no relation to scrapie and the evidence for a "slow infective" aetiology is very meagre. It is not related to an ageing process during which scrapie-like antigens make their appearance as they do in young animal with the disease. The emergence of scrapie-like antigens in ageing tissues is discussed. The increased sensitization of MS lymphocytes to scrapie, as opposed to normal brain (or spleen), is not characteristic of the disease, but occurs in other conditions with astroglial overgrowth. On the other hand, special lymphocyte sensitivity to inhibition by linoleic acid is limited to MS (and not shared by scrapie). The familial background of MS is briefly discussed, and an important line of study which might bring together classical genetic markers, HLA studies, and linoleic acid lymphocyte study is indicated. The role commonly ascribed to measles is critically reviewed. Measles may be of special importance in one (childhood-acquired) group of MS subjects, but there is no evidence of a special role in most cases. Raised antibodies to viruses other than measles have, however, been described. It is concluded that an immunological mechanism is still the most likely "final common path" by which MS lesions develop.