The pattern of Aβ deposition together with the lack of accompanying tau pathology differentiates the Aβ proteinopathy in iCJD from sporadic and genetic forms of AD; from that seen in young individuals without cognitive decline carrying one or two APOE4 alleles; from that in young genetic CJD patients with mutation in the PRNP gene; and from that related to TBI and CTE. This evidence concerns the gene MAPT and Creutzfeldt Jacob disease.