This conclusion is supported by our results showing that short-term memory and cognitive dysfunction in the APP/PS1 mouse model of AD is associated with a reduced ADAM17 expression in cerebral microvessels, whereas re-expression of ADAM17 restored endothelium-dependent vasodilator function in cerebral arteries and improved memory and cognitive function in the APP/PS1 mice. This evidence concerns the gene ADAM17 and Alzheimer disease.