Thus, increased oxidative stress from APOE4 astrocytes in the presence of Aβ leads to lack of neuronal support and consequent increased risk of neuron synaptic loss, contributing to a disease-promoting environment and increased risk for AD in APOE4 carriers (Corder et al., 1993; Farrer et al., 1997; Strittmatter & Roses, 1996). Here, APOE is linked to Alzheimer disease.