The genes and pathways identified here in our acute Aβ neurotoxicity models are also in contrast to genes strongly correlated with late-onset AD, including apolipoprotein E (APOE), triggering receptor expressed on myeloid cells 2 (TREM2) and cluster of differentiation 33 (CD33)21–24 among others, suggesting differences in gene regulation with early rises in Aβ in brain (prodromic period) as compared to AD. The gene discussed is APOE; the disease is Alzheimer disease.