SQSTM1 and Alzheimer disease: Studies conducted in vitro on transgenic mice and on the post-mortem brains of AD patients have demonstrated that the accumulation of C-terminal fragments of the amyloid precursor protein leads to defects in the selective removal of mitochondria (mitophagy), increasing the production of ROS and compromising the basic degradation of mitochondria, as indicated by the accumulation of p62/SQSTM1 [47].