While neprilysin overexpression was found to markedly reduce extracellular Aβ levels and, in fact, to completely eliminate all amyloid plaque formation in a robust APP transgenic mouse model (Mucke et al., 2000), levels of oligomeric forms of Aβ—an especially neurotoxic species strongly implicated in the AD pathogenesis—were found to be unchanged in these animals (Meilandt et al., 2009). The gene discussed is APP; the disease is Alzheimer disease.