Department of Autonomic Neuroscience, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakaecho, Itabashi-ku, Tokyo, 173-0015, Japan.
Animal Facility, Tokyo Metropolitan Institute of Gerontology, Tokyo, 173-0015, Japan.
J Physiol Sci. 2020 Dec 10;70(1):57. doi: 10.1186/s12576-020-00785-8.
Transient ischemia is an exacerbation factor of Alzheimer's disease (AD). We aimed to examine the influence of amyloid β (Aβ) deposition around the cerebral (pial) artery in terms of diameter changes in the cerebral artery during transient ischemia in AD model mice (APP) under urethane anesthesia. Cerebral vasculature and Aβ deposition were examined using two-photon microscopy. Cerebral ischemia was induced by transient occlusion of the unilateral common carotid artery. The diameter of the pial artery was quantitatively measured. In wild-type mice, the diameter of arteries increased during occlusion and returned to their basal diameter after re-opening. In AD model mice, the artery response during occlusion differed depending on Aβ deposition sites. Arterial diameter changes at non-Aβ deposition site were similar to those in wild-type mice, whereas they were significantly smaller at Aβ deposition site. The results suggest that cerebral artery changes during ischemia are impaired by Aβ deposition.
短暂性脑缺血是阿尔茨海默病（AD）的加重因素。我们旨在研究在 APP 模型小鼠（APP）乌来烷麻醉下短暂性脑缺血期间，脑动脉周围的淀粉样β（Aβ）沉积对脑动脉直径变化的影响。使用双光子显微镜检查脑血管和 Aβ沉积。通过短暂性阻塞单侧颈总动脉诱导脑缺血。定量测量脑动脉的直径。在野生型小鼠中，动脉在闭塞期间直径增加，在再开放后恢复到基础直径。在 AD 模型小鼠中，动脉在闭塞期间的反应取决于 Aβ沉积部位。非 Aβ 沉积部位的动脉直径变化与野生型小鼠相似，而 Aβ 沉积部位的动脉直径变化明显较小。结果表明，Aβ 沉积会损害脑缺血期间的脑动脉变化。
