XBP1 and Alzheimer disease: By contrast, activation of the IRE1 UPR branch appears to benefit AD pathogenesis, as shown in an AD model of Drosophila melanogaster, in which Xbp1 over-expression prevented Aβ toxicity (Casas-Tinto et al., 2011), as in a similar study in C. elegans, indicating that XBP1 is involved in defense against Aβ toxicity, presumably by increased autophagy (Safra et al., 2013).