Crosstalk between the ubiquitin-proteasome system and autophagy in a human cellular model of Alzheimer's disease

► Mutated AβPP increases oxidative stress and remodels the proteolysis in an AD model. ► Alterations in the autophagic flux are evident at the step of autophagosome formation. ► Cells try to counteract the altered scenario activating the HDAC6-dependent autophagy. ► Existence of an Aβ42 level beyond which proteolysis becomes definitely dysfunctional