However, whilst the interaction of Aβ with HSD10 causes a prompt increase in ROS levels, namely O2·− and H2O2, and a loss of mitochondria function [50], PreP activity was found to be decreased in AD brains and AD transgenic mouse brains, which also presented higher levels of oxidative products in their mitochondria [49]. The gene discussed is FSIP1; the disease is Alzheimer disease.