It has also been shown that in apoE4 carriers, the degree of glucose dysregulation (evaluated by fasting blood glucose concentration and mean glycemic value, as measured by the HbA1c concentration [59]) correlates with reduced cortical thickness and that apoE4 carriers with T2DM demonstrate a level of cortical thinning comparable to that of preclinical AD [60]. This evidence concerns the gene APOE and Alzheimer disease.