Further elevated plasma and brain ketone body levels could also affect AD via a variety of other mechanisms including (1) the blockade of Aβ1–42 (the toxic form of β-amyloid) entry into neurons which can decrease oxidative stress and amyloid burden [59] and (2) neuroprotection against β-amyloid toxicity possibly by decreasing ROS production and decreasing BACE1 expression, the rate-limiting enzyme in Aβ1–42 production [60]. Here, BACE1 is linked to Alzheimer disease.