Research conducted in multiple cellular and animal models strongly suggests that AD pathophysiology involves early changes in functionally connected networks across many brain regions that are not limited to cognition and learning [12]–[19] However, currently available biomarkers are limited to the measurements of tau, p-tau, and Aβ levels in CSF and plasma [20]–[22] that represent rather narrow hypothesis-driven biomarker development. This evidence concerns the gene MAPT and Alzheimer disease.