Relevant animal and cell experiments also showed that abnormally deposited Aβ can interfere with reduced coenzyme I (NADH) through Aβ-binding alcohol dehydrogenase (ABAD) in the mitochondria to affect the respiratory chain and increase ROS production, aggravating Aβ deposition and mitochondrial dysfunction to accelerate the formation of AD [37–39]. Here, HSD17B10 is linked to Alzheimer disease.