Moreover, it could be that this MFN2 variant partially alters localization of MFN2 [94], or interactions with other proteins, including PINK1 and PARKIN which, as mentioned above, are important mediators in the etiology of dementia, including Alzheimer’s disease (AD) and PD [95], or the variant may alter UQ biosynthesis or export to extramitochondrial endomembrane systems [89, 96]. This evidence concerns the gene PRKN and early-onset autosomal dominant Alzheimer disease.