The proposition of APOE as a likely candidate risk locus for AD was further supported by findings of reported interactions in vitro between ApoE and Aβ, but also evidence that people with APOE ε4 alleles, homozygotes in particular, appeared to have more pronounced vascular and Aβ plaque deposits than APOE ε3 carriers [90]. This evidence concerns the gene APOE and Alzheimer disease.