Journal
HYPERTENSION
Volume 79, Issue 3, Pages 629-637Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.121.18479
Keywords
aging; Alzheimer disease; blood pressure; dementia; tau protein
Categories
Funding
- National Institutes of Health/National Institute on Aging (NIH/NIA) [R01AG064228, R01AG060049, P50AG016573, P01AG052350]
- Alzheimer's Association [AARG-17532905]
- ADNI (Alzheimer's Disease Neuroimaging Initiative)
- National Institutes of Health [U01 AG024904]
- DOD ADNI (Department of Defense) [W81XWH-12-2-0012]
- National Institute on Aging
- National Institute of Biomedical Imaging and Bioengineering
- Alzheimer's Drug Discovery Foundation
- Araclon Biotech
- Biogen
- Bristol-Myers Squibb Company
- CereSpir, Inc
- Cogstate
- Eisai Inc
- Elan Pharmaceuticals, Inc
- Eli Lilly and Company
- EuroImmun
- F. Hoffmann-La Roche Ltd and its affiliated company Genentech, Inc
- Fujirebio
- GE Healthcare
- IXICO Ltd
- Janssen Alzheimer Immunotherapy Research & Development, LLC
- Lumosity
- Lundbeck
- Merck Co, Inc
- Meso Scale Diagnostics, LLC
- NeuroRx Research
- Neurotrack Technologies
- Novartis Pharmaceuticals Corporation
- Pfizer, Inc
- Piramal Imaging
- Servier
- Takeda Pharmaceutical Company
- Transition Therapeutics
- Canadian Institutes of Health Research
- BioClinica, Inc
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This study found that blood pressure variability (BPV) in older adults is related to tau accumulation in brain regions vulnerable to Alzheimer's disease, independent of average blood pressure levels. The relationship is modified by APOE ε4 carrier status. BPV may serve as a marker of vascular dysfunction contributing to early-stage tau pathology in Alzheimer's disease.
Background: Elevated blood pressure variability (BPV) is predictive of dementia, independent of average blood pressure levels, but neuropathological mechanisms remain unclear. We examined whether BPV in older adults is related to tau accumulation in brain regions vulnerable to Alzheimer disease and whether relationships are modified by apo epsilon 4 carrier status. Methods: Two hundred eighty-six Alzheimer's Disease Neuroimaging Initiative participants without history of dementia underwent 3 to 4 blood pressure measurements over 12 months and >= 1 tau positron emission tomography thereafter. BPV was calculated as variability independent of mean. Each scan determined tau burden (standardized uptake value ratio) for a temporal meta-region of interest, including burden from entorhinal cortex, amygdala, parahippocampus, fusiform, inferior temporal, and middle temporal. Bayesian linear growth modeling examined the role of BPV, apolipoprotein epsilon 4 carrier status, and time on regional tau accumulation after controlling for several variables, including baseline hypertension. Results: Elevated BPV was related to tau accumulation at follow-up in a temporal meta-region, independent of average blood pressure levels (ss, 0.89 [95% credible interval, 0.86-0.92]) and especially in entorhinal cortex (ss, 2.57 [95% credible interval, 2.15-2.99]). Apo epsilon 4 carriers with elevated BPV had the fastest tau accumulation at follow-up (ss, 1.73 [95% credible interval, 0.47-3.03]). Conclusions: BPV is related to tau accumulation in brain regions vulnerable to Alzheimer disease, independent of average blood pressure. APOE epsilon 4 modified this relationship. Bidirectionality of findings is possible. BPV may represent a marker of vascular dysfunction related to early-stage tau pathology contributing to Alzheimer disease.
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