Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Malmö, Sweden; Memory Clinic, Skåne University Hospital, Malmö, Sweden.
Department of Clinical Sciences Malmö, Clinical Memory Research Unit, Lund University, Malmö, Sweden; Department of Neurology, Skåne University Hospital, Lund, Sweden.
Alzheimers Dement. 2018 Jan;14(1):54-61. doi: 10.1016/j.jalz.2017.06.2265. Epub 2017 Jul 15.
It is hypothesized that cerebral hypoperfusion promotes the development of Alzheimer pathology. We therefore studied whether longstanding cerebral hypoperfusion is associated with Alzheimer pathology in nondemented humans.
Cerebral blood flow and amyloid β (F-Flutemetamol) positron emission tomography retention were assessed in eleven patients with unilateral occlusion of precerebral arteries resulting in chronic and uneven hypoperfusion. A subset of patients underwent tau (F-AV-1451) positron emission tomography.
The blood flow was significantly reduced on the affected side of the brain in patients with unilateral occlusion of the internal carotid artery or stenosis of the middle cerebral artery. However, the cortical uptake of F-Flutemetamol or F-AV-1451 was not altered.
Our results suggest that longstanding cerebral hypoperfusion in humans does not result in accumulation of amyloid β fibrils or tau aggregates.
据推测,脑灌注不足会促进阿尔茨海默病病理的发展。因此,我们研究了在非痴呆人群中,长期脑灌注不足是否与阿尔茨海默病病理有关。
对 11 例因大脑前循环动脉闭塞导致慢性、不均匀灌注不足的患者进行了脑血流和淀粉样蛋白 β(F-Flutemetamol)正电子发射断层扫描(PET)摄取的评估。部分患者进行了 tau(F-AV-1451)正电子发射断层扫描(PET)。
颈内动脉闭塞或大脑中动脉狭窄的患者大脑受影响侧的脑血流量显著降低,但 F-Flutemetamol 或 F-AV-1451 的皮质摄取没有改变。
我们的结果表明,人类长期脑灌注不足不会导致淀粉样蛋白 β 纤维或 tau 聚集物的积累。