Given converging data from studies on the initial cortical distribution of Alzheimer’s disease molecular pathology (Braak and Braak, 1991; Bejanin et al., 2017; Whitwell et al., 2018), with tau deposition in the EC and amyloid-β in the retrosplenial cortex, the path integration deficits observed here in prodromal Alzheimer’s disease may relate to a combination of tau and amyloid-β-related dysfunction in the EC and retrosplenial cortex, respectively. The gene discussed is MAPT; the disease is Alzheimer disease.