A commonly used Drosophila model of Alzheimer's disease generates an aberrant species of amyloid-beta with an additional N-terminal glutamine residue

Expression of human amyloid‐β (Aβ) in Drosophila is frequently used to investigate its toxicity in vivo. We expressed Aβ1–42 in the fly using a secretion signal derived from the Drosophila necrotic gene, as described in several previous publications. Surface‐enhanced laser desorption/ionization TOF MS analysis revealed that the Aβ produced contained an additional glutamine residue at the N‐terminus. AβQ+1–42 was found to have increased protein abundance and to cause more severe neurodegenerative effects than wild type Aβ1–42 as assessed by locomotor activity and lifespan assays. These data reveal that a commonly used model of Alzheimer's disease generates incorrect Aβ peptide.