In an APP transgenic (tg) mouse line (Tg2576) Aβ was also found to associate with mitochondria isolated from cerebral cortex [279]. It has also been reported that Aβ interacts with CyPD in mouse and human cerebral cortex mitochondria to potentiate synaptic stress [282]. Genetic deletion of CyPD (ppif) in human mutant APP tg mice (J-20 line) protects neurons from Aβ- and oxidative stress-induced cell death [282]. However, these abnormalities might not be related to the mPTP-driven cell death because these mice, and most other mouse models of AD, show scant or modest evidence for neurodegeneration resulting in neuronal cell death, despite tremendous brain burden of Aβ [283].