Abstract
A series of 15 different biochemical measurements were made on brains taken at stages throughout the development of scrapie and of transmissible mink encephalopathy in hamsters. With both diseases biochemical abnormalities were found only after the development of early histologic lesions, when animals showed clinical signs of disease. Changes were recorded in body weight, in the .activities of six glycosidases, and in the rates of incorporation of DNA and of glycoprotein precursors. The profiles of changes in hamster brain were almost indistinguishable, qualitatively and quantitatively, in the two diseases, an observation suggesting a close similarity in the way both disease-producing agents interact with this particular host species. However, there were some major differences between the profile of changes in hamster scrapie and that previously observed in mouse scrapie. Thus it would appear that many of the well-characterized abnormalities of mouse scrapie are not fundamentally involved in the development of disease but represent mainly secondary changes.