In addition, the acidic environment in mitochondria prevents Aβ clearanceowing to its rapid interaction with cyclophilin D (CypD) and/or Aβ-bindingalcohol dehydrogenase (ABAD) [147].ABAD is a mitochondrial protein that contributes to the toxic effect of Aβin mitochondria of AD patients and in a mouse model of AD by increasing ROSproduction and decreasing ATP levels [148, 149]. This evidence concerns the gene HSD17B10 and Alzheimer disease.