APP and amyloidosis: The measurement of urinary F(2)-isoprostanes, markers of free-radical damage22, has led to some particularly insightful clues into the basic biology of amyloidosis in mouse models of AD but also to the discovery that urinary levels of this component are greater in transgenic mice overexpressing human mutations of the amyloid precursor protein gene (APP), and that elevations in this component precede detectable Aβ plaque load23.