Thus, the increase in CSF eNOS observed in our cohort could reflect a compensative vasodilative mechanism put forward to counteract progressive Aβ-induced vasoconstriction in APOE ε3 patients, while such compensation seems to be lacking in carriers of ε4, indicating a possible regulatory role of the APOE genotype on the expression of NOS isoforms in AD. This evidence concerns the gene APOE and Alzheimer disease.