In 1995-96, 10 cases of CJD were identified in the United Kingdom (U.K.) with a new neuropathological profile. These cases were extremely unusual because of the young age of the patient, the clinical findings and the absence of the electroencephalogram features typical for CJD. Thus, the cases were found to represent a new variant of CJD and the possibility that they were casually linked to BSE began to be researched.5

Research conducted to support the possibility that vCJD and BSE were somehow linked found that variant CJD had strain characteristics distinct from other types of CJD and which resembled those of BSE that had been transmitted to mice, domestic cats and macaque.6

The link has now been convincingly established in laboratory studies showing distinctive biological and molecular biological features of the disease-causing prion protein (PrPSc) isolated from BSE-infected cattle and human cases of vCJD.7

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