BACE1 and Alzheimer disease: While these mechanistic studies were all in animals or on cell lines expressing human BACE1, the level of BACE1 and its enzymatic activity are increased in humans suffering from AD [78], as expected from the fact that the capillary constriction in humans developing AD is sufficient to reduce cerebral blood flow by up to 50% [133] and the animal work cited above showing that ischaemia and hypoxia upregulate BACE1.