Department of Translational Neuroscience, The Mind Research Network, Albuquerque, New Mexico, USA.
Nene and Jamie Koch Comprehensive Movement Disorder Center, Department of Neurology, University of New Mexico, Albuquerque, New Mexico, USA.
Mov Disord. 2023 Jul;38(7):1262-1272. doi: 10.1002/mds.29429. Epub 2023 May 8.
Cerebrovascular dysfunction in Parkinson's disease (PD) is heterogeneous and may contribute to disease pathophysiology or progression. There is a need to understand the mechanisms by which cerebrovascular dysfunction is altered in participants with PD.
The objective of this study is to test the hypothesis that participants with PD exhibit a significant reduction in the ability of the cerebral vessels to dilate in response to vasoactive challenges relative to healthy controls (HC).
The current study uses a vasodilatory challenge while participants undergo functional magnetic resonance imaging to quantify the amplitude and delay of cerebrovascular reactivity in participants with PD relative to age and sex-matched HC. An analysis of covariance was used to evaluate differences in cerebrovascular reactivity amplitude and latency between PD participants and HC.
A significant main effect of group was observed for whole-brain cerebrovascular reactivity amplitude (F = 4.38, p = 0.046, Hedge's g = 0.73) and latency (F = 16.35, p < 0.001, Hedge's g = 1.42). Participants with PD exhibited reduced whole-brain amplitude and increased latencies in cerebrovascular reactivity relative to HC. The evaluation of regional effects indicates that the largest effects were observed in the cuneus, precuneus, and parietal regions.
PD participants exhibited reduced and delayed cerebrovascular reactivity. This dysfunction may play an important role in chronic hypoxia, neuroinflammation, and protein aggregation, mechanisms that could lead to disease progression. Cerebrovascular reactivity may serve as an important biomarker and target for future interventions. © 2023 The Authors. Movement Disorders published by Wiley Periodicals LLC on behalf of International Parkinson and Movement Disorder Society.
帕金森病(PD)患者的脑血管功能存在异质性,可能导致疾病的病理生理学或进展。需要了解 PD 患者脑血管功能改变的机制。
本研究旨在检验以下假设:与健康对照(HC)相比,PD 患者的脑血管在对血管活性挑战做出反应时,其扩张能力显著降低。
本研究使用血管扩张性挑战,同时让参与者进行功能磁共振成像,以量化 PD 参与者相对于年龄和性别匹配的 HC 的脑血管反应性的幅度和延迟。采用协方差分析评估 PD 参与者和 HC 之间的脑血管反应性幅度和潜伏期的差异。
观察到全脑脑血管反应性幅度(F = 4.38,p = 0.046,Hedge's g = 0.73)和潜伏期(F = 16.35,p < 0.001,Hedge's g = 1.42)的组间存在显著主效应。与 HC 相比,PD 参与者的全脑脑血管反应性幅度降低,潜伏期延长。对区域效应的评估表明,在楔前叶、楔叶和顶叶区域观察到最大的效应。
PD 参与者表现出脑血管反应性降低和延迟。这种功能障碍可能在慢性缺氧、神经炎症和蛋白质聚集的机制中发挥重要作用,这些机制可能导致疾病进展。脑血管反应性可能作为一个重要的生物标志物和未来干预的靶点。© 2023 作者。运动障碍由 Wiley 期刊公司代表国际帕金森病和运动障碍协会出版。