Relationship between cerebral perfusion/neuronal activity and amyloid deposition

已经认为脑血流量减少可能加速阿尔茨海默病（AD）相关的病理。为探讨局部脑血流量（rCBF）降低对β淀粉样蛋白（A β）沉积形成的影响，采用左侧颈总动脉结扎法建立淀粉样前体蛋白转基因（APP Tg）小鼠单侧脑低灌注模型。使用[11 C]PIB-PET和MRI在数月内定量监测Abeta沉积和rCBF的进展。同侧新皮层的rCBF维持对侧新皮层的84%。随着时间的推移，Abeta沉积增加并扩大，而没有与灌注不足相关的偏侧性。目前的研究结果表明，慢性脑灌注不足并不被认为是加速A β斑块的沉积。在活体成像技术，如PET和MRI具有优势，以纵向观察活体模型小鼠脑中的A 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.