On the other hand, in Aβ-based AD models, the genetic deletion of the fission-inducer Drp1 rescued from mitochondrial fragmentation, the drop of mitochondrial membrane potential and ATP production, the generation of ROS in vitro and prevented the accumulation of lipid peroxidation products, beta-secretase 1 expression, the formation of amyloid plaques and cognitive decline in APPswe/PSEN1dE9 mice (Baek et al., 2017). This evidence concerns the gene DNM1L and Alzheimer disease.