Alterations in vascular reactivity in single-and double-transgenic mice coexpressing human APP-C100 and mutant SOD_1 gene

摘要

Conclusions The present study suggests that the altered reactivity of the microvasculature may be mediated by circulating soluble Aβpeptides. The mechanisms underlying the vasoactivity of circulating Aβin TgC100 and double Tg mice involve both the endothelium and nonendothelium. Objective To explore the mechanism underlying changes in microvascular reactivity in single-and double- Transgenic mice. Methods Peripheral vascular reactivity to the vasodilators, acetylcholine and sodium nitroprusside, on Perfused microvasculature of the hind footpad was investigated using nontransgenic mice, single-transgenic Mice expressing the human APP-C10(TgC100. WT or TgC100.V717F)and double-transgenic mice Coexpressing human APP-C100 and human SOD_1(G93A)genes.