Beginning at 3 months of age, Kir6.2+/+ APP/PS1 and Kir6.2–/– APP/PS1 mice were exposed to high-sucrose drinking water (e.g., sugar H2O) or normal drinking water for 6 months to assess the role of Kir6.2-dependent KATP channels in glucose-dependent amyloid plaque formation and AD-related pathology (n = 8–11 mice/group; Figure 6A). Here, KCNJ11 is linked to Alzheimer disease.