Platelet-activating factor (PAF)-mediated hydrolysis of cholesterol esters stabilizes amyloid-beta (Aβ)-containing lipid rafts. Schematic demonstrating the putative mechanism regulating the formation of Aβ-containing rafts. In this theory, Aβ42 activates cPLA2, resulting in the production of PAF. PAF activates cholesterol ester hydrolase (CEH) and the release of cholesterol from stores of cholesterol esters, which stabilizes Aβ42 in rafts. Inhibition of cPLA2 (arachidonyl trifluoromethyl ketone, or AACOCF3), antagonism of the PAF receptors (Hexa-PAF), or inhibition of CEH (diethylumbelliferyl phosphate, is DEUP) reduces the cholesterol concentrations in the endoplasmic reticulum (ER). cPLA2, cPLA2 is cytoplasmic phospholipase A2; Hexa-PAF, 1-O-hexadecyl-2-acetyl-sn-glycerol-3-phospho-(N,N,N-trimethyl)-hexanolamine.