Associations of longitudinal blood pressure with cerebral amyloid angiopathy in older adults

Blood pressure (BP) and cerebral amyloid angiopathy (CAA) are both risk factors for age-related cognitive decline, yet their associations are incompletely investigated. Here, we investigated the associations between longitudinal BP and neocortical CAA scores in 2107 older adults (mean age, 89.63 years) who were followed in one of five longitudinal cohort studies of aging. Systolic BP (SBP), diastolic BP (DBP), mean arterial pressure (MAP) and pulse pressure (PP) were collected at baseline and annual clinical visits whereas CAA and Alzheimer’s disease (AD) were assessed at autopsy.

This study is a secondary analysis of the prospectively collected clinical and postmortem data from the five cohort studies. Logistic regression was used to analyze the association of mean BP across time with moderate-to-severe CAA. In primary analyses, we evaluated CAA in composite neocortex.

In secondary analyses, we explored CAA in specific neocortical brain regions (i.e., frontal, temporal, parietal, and occipital) and controlled for cohort as well as CAA risk factors including APOE genotype and presence of AD pathology. All models adjusted for age at death, sex, and education. Primary regression analyses demonstrated no association between mean BP and moderate-to-severe CAA in the composite neocortex.

However, secondary analyses revealed a weak inverse association between mean PP and moderate-to-severe CAA in the frontal neocortex (OR, 0.991 [95% CI, 0.983–0.998]) that remained after controlling for presence of AD and APOE genotype. We conclude that mean BP is not associated with CAA in composite neocortex, however further research into the associations of specific BP values with CAA severity may be warranted and should consider specific brain regions. The authors thank all the research participants in the cohort studies at the RADC for their altruism and commitment to research.

The authors also thank the RADC staff and faculty, in particular Ryan Johnson for laboratory management; Shayla Calloway, Traci Colvin, Theresa Mathes, Elizabeth Montalvo, and Tracey Nowakowski for study coordination; John Gibbons for data management; and Jennifer Cheng and Michelle Jones for statistical programming. This work was supported by grants from the NIH grants: RF1AG083765, R01AG017917, R01AG022018, R01NS084965, RF1AG059621, RF1AG074549, P30AG10161, P30AG072975, R01AG15819. Rush Alzheimer’s Disease Center, Rush University Medical Center, 1750 W Harrison Street, Chicago, IL, 60612, USA Rupal I.

Bennett & Zoe Arvanitakis Department of Neurology, The University of Chicago, Chicago, IL, 60637, USA T.H. Chan School of Public Health, Harvard University, Boston, MA, 02115, USA All authors declare no competing interests. Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.