APP and Alzheimer disease: Overexpression and mislocation of tau proteins appear to modulate kinesin-1 based transport [147,241] by direct inhibition of motors on microtubule tracts, and this can lead to transport disruption for numerous cargoes, including APP vesicles, mitochondria, and peroxisomes, which could explain the energy deprivation and the oxidative stress sensitivity of AD neurons [249,254].