Despite this limitation, we were struck by the high degree of preservation between transcriptional networks of tau transgenic mice and sporadic human Alzheimer’s disease, as well as conservation of Moesin elevation in tau transgenic Drosophila. In addition, while analyses in tau transgenic Drosophila reveal a tight co-incidence of Moesin elevation and cell cycle activation as detected by PCNA, future neuropathological analyses of human Alzheimer’s disease brain are required to determine if Moesin activation and aberrant cell cycle activation are tightly linked in the human condition. This evidence concerns the gene MSN and early-onset autosomal dominant Alzheimer disease.