Takechi Ryusuke, Galloway Susan, Pallebage-Gamarallage Menuka, Wellington Cheryl, Johnsen Russell, Mamo John Charles
Centre for Metabolic Fitness, School of Public Health, Curtin Health Innovative Research Institute, Curtin University of Technology, GPO Box U1987, Building 400, Bentley Campus, Perth, WA, 6845, Australia.
Histochem Cell Biol. 2009 May;131(5):661-6. doi: 10.1007/s00418-009-0567-3. Epub 2009 Feb 19.
Parenchymal accumulation of amyloid-beta (A beta) is a hallmark pathological feature of Alzheimer's disease. An emerging hypothesis is that blood-to-brain delivery of A beta may increase with compromised blood-brain barrier integrity. In plasma, substantial A beta is associated with triglyceride-rich lipoproteins (TRLs) secreted by the liver and intestine. Utilizing apolipoprotein B as an exclusive marker of hepatic and intestinal TRLs, here we show utilizing an highly sensitive 3-dimensional immuno-microscopy imaging technique, that in APP/PS1 amyloid transgenic mice, concomitant with substantially increased plasma A beta, there is a significant colocalization of apolipoprotein B with cerebral amyloid plaque. The findings are consistent with the possibility that circulating lipoprotein-A beta contributes to cerebral amyloidosis.
淀粉样β蛋白（Aβ）在脑实质中的蓄积是阿尔茨海默病标志性的病理特征。一个新出现的假说是，随着血脑屏障完整性受损，Aβ的血脑转运可能会增加。在血浆中，大量Aβ与肝脏和肠道分泌的富含甘油三酯的脂蛋白（TRL）相关联。利用载脂蛋白B作为肝脏和肠道TRL的唯一标志物，我们在此使用一种高度灵敏的三维免疫显微镜成像技术表明，在APP/PS1淀粉样蛋白转基因小鼠中，伴随着血浆Aβ显著增加，载脂蛋白B与脑淀粉样斑块存在明显的共定位。这些发现与循环脂蛋白 - Aβ导致脑淀粉样变性的可能性一致。
