The idea of undertaking a combined genetic analysis of sporadic AD and sCJD searching for interactions was motivated by reports on: i) the potential role of PrP in AD [35]–[41], and ii) because as brain amyloidoses, AD and sCJD, share several epidemiologic features such as an age at onset concordant with the clinical course duration, and vascular risk factors well established for AD and recently suggested for sCJD [3], [42], [43]. The gene discussed is PRNP; the disease is Alzheimer disease.