The fact that aggregated Aβ (not mAβ) reduces induction of ABCC1 expression supports the hypothesis that in the early stage of AD, less aggregated Aβ increases GSH release from astrocytes (via ABCC1 transporters and Cx43 HCs) providing temporary protection from oxidative stress that promotes AD development [512]. The gene discussed is GJA1; the disease is Alzheimer disease.