Our null findings could inform models of the spatio-temporal ordering of alterations within the PMC of APOE E4 carriers that predispose to earlier amyloid accumulation in this region and ultimately development of AD, suggesting that resting PMC neurotransmitter differences do not occur prior to PMC functional changes that are observed in young adult APOE E4 carriers in this region. Here, APOE is linked to amyloidosis.