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Chronic cerebral hypoperfusion did not accelerate [11C]PIB-reactive Abeta deposition in amyloid precursor protein transgenic mice.

https://repo.qst.go.jp/records/65044
https://repo.qst.go.jp/records/65044
2f279523-c7ae-4f07-9673-0d3289fe91f3
Item type 会議発表用資料 / Presentation(1)
公開日 2013-06-17
タイトル
タイトル Chronic cerebral hypoperfusion did not accelerate [11C]PIB-reactive Abeta deposition in amyloid precursor protein transgenic mice.
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_c94f
資源タイプ conference object
アクセス権
アクセス権 metadata only access
アクセス権URI http://purl.org/coar/access_right/c_14cb
著者 Seki, Chie

× Seki, Chie

WEKO 640961

Seki, Chie

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Higuchi, Makoto

× Higuchi, Makoto

WEKO 640962

Higuchi, Makoto

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Tokunaga, Masaki

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WEKO 640963

Tokunaga, Masaki

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Maruyama, Masahiro

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WEKO 640964

Maruyama, Masahiro

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Ono, Maiko

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WEKO 640965

Ono, Maiko

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Ki, Hin

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WEKO 640966

Ki, Hin

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Maeda, Jun

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WEKO 640967

Maeda, Jun

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Nitta, Nobuhiro

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WEKO 640968

Nitta, Nobuhiro

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Aoki, Ichio

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WEKO 640969

Aoki, Ichio

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Suhara, Tetsuya

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WEKO 640970

Suhara, Tetsuya

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Ito, Hiroshi

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WEKO 640971

Ito, Hiroshi

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関 千江

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en 関 千江

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樋口 真人

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en 樋口 真人

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徳永 正希

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WEKO 640974

en 徳永 正希

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丸山 将浩

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en 丸山 将浩

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小野 麻衣子

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WEKO 640976

en 小野 麻衣子

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季 斌

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前田 純

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en 前田 純

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青木 伊知男

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須原 哲也

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伊藤 浩

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抄録
内容記述タイプ Abstract
内容記述 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)
内容記述タイプ Other
内容記述 XXVIth International Symposium on Cerebral Blood Flow, Metabolism and Function
発表年月日
日付 2013-05-23
日付タイプ Issued
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