This mitochondrial mislocalization exacerbated by Miro mutation ultimately enhances Aβ42-induced behavioral deficits in Drosophila. Moreover, knockdown of Miro in AD model flies has been reported to enhance the tau-induced neurodegeneration by increasing the tau phosphorylation in AD-related site S262 by PAR1 kinase (Iijima-Ando et al., 2012), suggesting that Miro might play an important role in the modulation of AD-related pathologies. Here, MAPT is linked to Alzheimer disease.