Indeed, the exposure of cultured brain-derived endothelial cells to inhibitors of NO production including the peptide A beta (a compound largely involved in the physiopathology of Alzheimer disease) and ADMA (an endogenous eNOS inhibitor) was reported to decrease BDNF production (Guo et al., 2008; Ma et al., 2015). The gene discussed is BDNF; the disease is early-onset autosomal dominant Alzheimer disease.