Relationship between cerebral perfusion/neuronal activity and amyloid deposition

人们一直认为脑血流量减少可能加速阿尔茨海默病（AD）相关病理。为了研究区域脑血流量（rCBF）降低对淀粉样蛋白（Abeta）沉积形成的影响，我们通过结扎左颈总动脉，建立了淀粉样蛋白前体蛋白转基因（APP Tg）小鼠单侧脑低灌注模型。在几个月内用[11C]PIB-PET和MRI定量监测β沉积和rCBF的进展。同侧新皮层的rCBF可达对侧新皮层的84%。随着时间的推移，β沉积增加和扩大，没有与低灌注相关的侧边。目前的结果表明，慢性脑灌注不足不被认为会加速β斑块的沉积。PET和MRI等体内成像技术有利于纵向观察活模型小鼠大脑中β沉积和rCBF的变化。

It has been considered that decreased cerebral blood flow may accelerate Alzheimer's disease (AD) related pathologies. To investigate the impact of lowered regional cerebral blood flow (rCBF) on the formation of amyloid beta (Abeta) deposition, unilateral cerebral hypoperfusion model was made on amyloid precursor protein transgenic (APP Tg) mice by the ligation of the left common carotid artery. The progression of Abeta depositions and rCBF were quantitatively monitored with [11C]PIB-PET and MRI over months. The rCBF of ipsilaterel neocortex sustained up to 84% of that of contralateral neocortex. The Abeta deposition increased and expanded over time without laterality related to hypoperfusion. The current results indicate that chronic cerebral hypoperfusion is not considered to accelerate deposition of Abeta plaques.In vivo imaging technologies such as PET and MRI have advantageous to visualize alterations of Abeta depositions and rCBF in living model mouse brains longitudinally.