量研学術機関リポジトリ「QST-Repository」は、国立研究開発法人 量子科学技術研究開発機構に所属する職員等が生み出した学術成果（学会誌発表論文、学会発表、研究開発報告書、特許等）を集積しインターネット上で広く公開するサービスです。 Welcome to QST-Repository where we accumulates and discloses the academic research results(Journal Publications, Conference presentation, Research and Development Report, Patent, etc.) of the members of National Institutes for Quantum Science and Technology.
Thank you very much for using our website. On the 11th of March 2019, this site was moved from our own network server to the JAIRO Cloud network server. If you previously bookmarked this site, that bookmark will no longer work. We would be grateful if you could bookmark the website again. Thank you very much for your understanding and cooperation.
Introduction Mild cerebral hypoperfusion events are relevant in aged individuals. It has been reported that decreased cerebral blood flow can accelerate Alzheimer's disease (AD) related pathologies but the underlying mechanism has been still unclear. [11C]PIB is a PET imaging probe for Abeta plaques and [11C]PIB-PET can also detect the progression of Abeta amyloidosis with aging in living AD model mice1. Therefore the application of this method to an AD animal model with local cerebral hypoperfusion would reveal the impact of lowered regional cerebral blood flow (rCBF) on the Abeta plaque formation in living brains. In this study, unilateral hypoperfusion model was made on amyloid precursor protein transgenic (APP Tg) mice, and repeated [11C]PIB-PET scans were performed to observe the progression of Abeta depositions and MRI scans for monitoring rCBF and ischemic infarction.
Methods All of the following animal procedures were performed under anesthesia with 1.5% (v/v) isoflurane. The left common carotid artery (lCCA) of an APP Tg mouse aged 18-20 months (n=3) was isolated from the adjacent vagus nerve and doubly ligated with a 6-0 silk suture. MRI scans with a 7T scanner were performed to evaluate rCBF with flow sensitive alternating inversion recovery method and formation of cerebral infarction with T2-weighted (T2W) and diffusion tensor imaging. [11C]PIB-PET and MRI scans were performed 2 weeks before the ligation as the baseline, then repeatedly at 3 days to 4 or 6 months after the ligation to monitor longitudinal alternations of rCBF alternations and Abeta deposition. The distribution of Abeta deposition was evaluated with standardized uptake ratio (SUVR) map of [11C]PIB-PET data averaged at 40-60 min using the cerebellum as a reference region.
Results and Conclusion The relative reduction of rCBF of ipsilateral neocortex by lCCA ligation was 42-58 % of contralateral neocortex at 3 days post ligation, then gradually increased up to 90 % after 6 months. There was no ischemic infarction observed in all animals based on the inspection of T2W images and apparent diffusion coefficient maps. The Abeta deposition increased and expanded over time without laterality related to hypoperfusion. The current results indicate that chronic cerebral hypoperfusion without formation of ischemic infarction detectable by MRI does not accelerate deposition of [11C]PIB-reactive Abeta plaques.
\n1)Maeda J, et al., J Neurosci ; 27(41):10957-68, 2007
会議概要（会議名, 開催地, 会期, 主催者等）
XXVIth International Symposium on Cerebral Blood Flow, Metabolism and Function
Chronic cerebral hypoperfusion did not accelerate [11C]PIB-reactive Abeta deposition in amyloid precursor protein transgenic mice.
