INS and Alzheimer disease: Prior studies have reported altered allostatic markers in AD,26,28–31 noting that cardiometabolic burden may have a more substantial impact on AD risk than genetic factors.5 Therefore, a plausible mechanism underlying this disruption in AD is impaired insulin signaling in the brain.29 Impaired insulin signaling has a bidirectional relationship with allostatic load and has been proposed to exacerbate AD pathophysiology,29 particularly within the hippocampus78 and in more vulnerable populations29 similar to our patient cohort.