In contrast, it has been shown that OPA1 overexpression effectively preserves mitochondrial integrity prevents cytochrome c release, protecting cells against apoptotic stimuli in prion disease models in vitro and in vivo [41].These mechanisms may partially overlap with the pathological features observed in AD, particularly mitochondrial dysfunction, energy failure, synaptic dysfunction and neuronal loss,. Here, OPA1 is linked to Alzheimer disease.