At a molecular level, James Duce (University of Leeds, UK) presented evidence that iron disruption in AD could be modulated by the processing of amyloid precursor protein (APP) on the cell surface whereby the amyloidogenic pathway that requires BACE1 and leads to Aβ generation also causes intraneuronal iron retention and increases vulnerability to reactive oxygen species neurotoxicity; a common concomitant in AD. The gene discussed is APP; the disease is Alzheimer disease.