Chronic hypoperfusion due to intracranial large artery stenosis is not associated with cerebral β-amyloid deposition and brain atrophy. Issue 5 (5th March 2022)

• Record Type: Journal Article
• Authors: Fan, Dongyu; Li, Huiyun; Chen, Dongwan; Chen, Yang; Yi, Xu; Yang, Heng; Shi, Qianqian; Jiao, Fangyang; Tang, Yi; Li, Qiming; Wang, Fangyang; Wang, Shunan; Jin, Rongbing; Zeng, Fan; Wang, Yanjiang
• Editors: Yin, Yanjie; Hao, Xiuyuan
• Is Part Of: Chinese medical journal. Volume 135:Issue 5(2022)
• Page Start: 591
• Page End: 597
• Publication Date: 2022-03-05
• Subjects: Cerebral hypoperfusion -- β-amyloid -- Brain atrophy -- Alzheimer disease; Medicine -- Periodicals; Medicine, Oriental -- Periodicals; Medicine; Medicine, Oriental; Medicine; Medicine, East Asian Traditional; Periodicals; Electronic journals; 610.5
• DOI: 10.1097/CM9.0000000000001918
• Languages: English
• ISSNs: 0366-6999

Abstract

Abstract: Background: Insufficient cerebral perfusion is suggested to play a role in the development of Alzheimer disease (AD). However, there is a lack of direct evidence indicating whether hypoperfusion causes or aggravates AD pathology. We investigated the effect of chronic cerebral hypoperfusion on AD-related pathology in humans. Methods: We enrolled a group of cognitively normal patients (median age: 64 years) with unilateral chronic cerebral hypoperfusion. Regions of interest with the most pronounced hypoperfusion changes were chosen in the hypoperfused region and were then mirrored in the contralateral hemisphere to create a control region with normal perfusion. 11 C-Pittsburgh compound-positron emission tomography standard uptake ratios and brain atrophy indices were calculated from the computed tomography images of each patient. Results: The median age of the 10 participants, consisting of 4 males and 6 females, was 64 years (47–76 years). We found that there were no differences in standard uptake ratios of the cortex (volume of interest [VOI]: P = 0.721, region of interest [ROI]: P = 0.241) and grey/white ratio (VOI: P = 0.333, ROI: P = 0.445) and brain atrophy indices (Bicaudate, Bifrontal, Evans, Cella, Cella media, and Ventricular index, P > 0.05) between the hypoperfused regions and contralateral normally perfused regions in patients with unilateral chronic cerebral hypoperfusion. Conclusion: Our findings suggest that chronic hypoperfusion due to large vessel stenosis may not directly induce cerebral β-amyloid deposition and neurodegeneration in humans.