While it is conceivable that ADMA here is serving only as a marker for vascular pathology that might work in other ways to promote development of AD, rodent and cell culture studies suggest that microvascular eNOS activity may function to restrain the expression of both amyloid precursor protein and beta-secretase in brain parenchyma and vasculature—thereby suppressing production of amyloid beta—and also to down-regulate microglial activation. The gene discussed is NOS3; the disease is Alzheimer disease.