In our previous study, we showed that processes related to AD such as increased production of Aβ, unbalanced production of Aβ fragments favoring Aβ1–42 or oligomerization of Aβ1–42 significantly affect the interactions between Aβ and mitochondrial proteins and enhance the binding of Aβ1–42 to both cypD and 17β-HSD10 [23]. This evidence concerns the gene HSD17B10 and Alzheimer disease.