Interestingly, recent reports that increased mitochondrial ROS generation associated with both high glucose exposure in human endothelial cells and Alzheimer’s disease in mouse hippocampal tissue, is attenuated by GLP-1(9–36) [21, 46, 47], suggest that such antioxidant actions of GLP-1(9–36) may underlie the observed attenuation of post-MI remodelling, specific components of which are known to be significantly influenced by ROS [48]. The gene discussed is GLP1R; the disease is early-onset autosomal dominant Alzheimer disease.