We measured ACE-2 activity by fluorogenic peptide substrate assay in mid-frontal cortex (Brodmann area 9) in a cohort of AD (n = 90) and age-matched non-demented controls (n = 59) for which we have previous data on ACE-1 activity, amyloid β (Aβ) level and tau pathology, as well as known ACE1 (rs1799752) indel polymorphism, apolipoprotein E (APOE) genotype, and cerebral amyloid angiopathy severity scores.
In a case-control study including 376 late-onset AD patients and 444 control subjects, we showed a statistically significant effect on the risk of AD of tw</span>o variants (rs4343 and rs1799752) and of the haplotype ATI (rs4343/rs4291/rs1799752) in subjects aged 73 years and above.