Key result
Higher diastolic BP variability is linked to increased longitudinal brain tau accumulation in Alzheimer-vulnerable regions.
Why the study?
Elevated blood pressure variability predicts dementia independently of average blood pressure, but the underlying neuropathological mechanisms remain unclear.
Does elevated visit-to-visit blood pressure variability predict longitudinal tau accumulation in older adults without dementia?
Cohort (n=286)
Yes
Does elevated visit-to-visit blood pressure variability predict longitudinal tau accumulation in older adults without dementia?
Effect estimate: ß 0.89 (95% CI 0.86-0.92)
Elevated visit-to-visit blood pressure variability is linked to increased early-stage tau pathology in Alzheimer's disease brain regions, particularly among APOEϵ4 carriers.
Should not yet change BP management in older adults; leaves open whether visit-to-visit variability influences early tau accumulation.
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 apoϵ4 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 ϵ4 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]). Apoϵ4 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. APOEϵ4 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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Sible et al. (2021) conducted a cohort in Without history of dementia (cognitively normal or mild cognitive impairment) (n=286). Elevated visit-to-visit blood pressure variability vs. Lower visit-to-visit blood pressure variability was evaluated on Tau accumulation (standardized uptake value ratio) at follow-up in a temporal meta-region (ß 0.89, 95% CI 0.86-0.92). Elevated visit-to-visit diastolic blood pressure variability was associated with increased longitudinal tau accumulation in temporal brain regions vulnerable to early-stage Alzheimer disease (ß 0.89).
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