Thus, these studies highlight that IGF-1 signaling in the brain—and its effects on diverse cell types, physiological processes, and disease states, including AD—is inherently complex, with outcomes that can be influenced by sex, species, and other nuances, making it unlikely that IGF-1 action in the brain simply conforms to a “one-size-fits-all” description. This evidence concerns the gene IGF1 and Alzheimer disease.