Research Paper Volume 12, Issue 18 pp 18221—18237
High pulse pressure is a risk factor for prodromal Alzheimer’s disease: a longitudinal study
- 1 Department of Neurology, Qingdao Municipal Hospital, Dalian Medical University, Dalian, China
- 2 College of Medicine and Pharmaceutics, Ocean University of China, Qingdao, China
- 3 Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China
- 4 Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China
- 5 Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, China
Received: February 18, 2020 Accepted: June 29, 2020 Published: September 22, 2020
https://doi.org/10.18632/aging.103678How to Cite
Copyright: © 2020 Shi et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
It has been increasingly evident that pulse pressure (PP) is associated with Alzheimer's disease (AD) but whether PP increases AD risk and the mechanism responsible for this association remains unclear. To investigate the effects of PP in the process of AD, we have evaluated the cross-sectional and longitudinal associations of PP with AD biomarkers, brain structure and cognition and have assessed the effect of PP on AD risk in a large sample (n= 1,375) from the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Multiple linear regression and mixed-model regression were employed in cross-sectional and longitudinal analyses respectively. Clinical disease progression was assessed using Cox proportional hazards models. High PP was associated with lower β-amyloid 42 (Aβ42) (P= .015), and higher total tau (T-tau) (P= .011), phosphorylated tau (P-tau) (P= .003), T-tau/Aβ42 (P= .004) and P-tau/Aβ42 (P = .001), as well as heavier cortical amyloid-beta burden (P= .011). Longitudinally, baseline high PP was significantly associated with hippocampal atrophy (P= .039), entorhinal atrophy (P= .031) and worse memory performance (P= .058). Baseline high PP showed more rapid progression than those with normal PP (P <.001). These results suggest PP elevation could increase AD risk, which may be driven by amyloid plaques and subclinical neurodegeneration.