Likewise, transgenic mice expressing AD-related mutant forms of amyloid-beta precursor protein (APP) and presenilin (PS1) have been reported to exhibit Aβ-related mitochondrial Ca2+ overload, that is ameliorated upon MCU inhibition, while pathological forms of tau have been shown to inhibit NCLX, further sensitizing mitochondria to Ca2+ overload229,230. This evidence concerns the gene APP and Alzheimer disease.