Studies on transgenic mice and AD patients confirmed that Aβ can directly interact with MITO Aβ-binding alcohol dehydrogenase (ABAD) leading to increased ROS generation, MITO dysfunction and cell death [146]; inhibition of the ABAD–Aβ interaction in a mouse model attenuated Aβ accumulation, conserved MITO function and improved spatial learning in an AD animal model [147]. The gene discussed is HSD17B10; the disease is Alzheimer disease.