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Research Paper|Volume 12, Issue 18|pp 18221—18237

High pulse pressure is a risk factor for prodromal Alzheimer’s disease: a longitudinal study

Wen-Yan Shi1, Zuo-Teng Wang2, Fu-Rong Sun3, Ya-Hui Ma3, Wei Xu3, Xue-Ning Shen4, Qiang Dong4, Lan Tan1,2,3, Jin-Tai Yu4, Yang Yu5, Alzheimer’s Disease Neuroimaging Initiative
  • 1Department of Neurology, Qingdao Municipal Hospital, Dalian Medical University, Dalian, China
  • 2College of Medicine and Pharmaceutics, Ocean University of China, Qingdao, China
  • 3Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao, China
  • 4Department of Neurology and Institute of Neurology, Huashan Hospital, Shanghai Medical College, Fudan University, Shanghai, China
  • 5Department of Neurology, The Affiliated Hospital of Qingdao University, Qingdao, China
* Data used in preparation of this article were obtained from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database (http://adni.loni.usc.edu). As such, the investigators within the ADNI contributed to the design and implementation of ADNI and/or provided data but did not participate in analysis or writing of this report. A complete listing of ADNI investigators can be found at: http://adni.loni.usc.edu/wp-content/uploads/how_to_apply/ADNI_Acknowledgement_List.pdf
Received: February 18, 2020Accepted: June 29, 2020Published: September 22, 2020
https://doi.org/10.18632/aging.103678

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.