Given that Aβ directly impairs mitochondrial enzyme function and that AD is associated with impaired glucose metabolism we hypothesized that manipulating APP processing through BACE1 overexpression in SH-SY5Y neuroblastoma cells would phenocopy the defects in glucose metabolism at the cellular level, allowing us to explore in more detail this initial and potentially causative change in AD progression. The gene discussed is APP; the disease is Alzheimer disease.