Given that DLP1 and Mfn2 are substrates of calpain and cleaved by calpain activation induced by multiple AD-relevant insults in vitro [106], the fact that reduced levels of these GTPases correlated with calpain activation in AD brain suggests that calpain-mediated degradation could at least contribute to the reduction of these fission/fusion GTPases in AD [106]. Here, MFN2 is linked to Alzheimer disease.