In the same APP-transgenic mouse strain as we used in this study, another group has reported that the absence of gut bacteria increased protein levels of Aβ-degrading enzymes neprilysin and Ide.8 However, our study showed that depletion of intestinal bacteria altered neither Neprilysin nor Ide gene transcription in the brains of Il-17a-deficient and wildtype APP-transgenic mice (Figure 7, g–j; t test, p > 0.05), which suggested that extracellulardegradation of Aβ was not the mechanism mediating Aβ reduction in our AD mice. The gene discussed is IL17A; the disease is Alzheimer disease.