1. Increased measures of systemic arterial stiffness were found to be significantly associated with a greater extent of β-Amyloid deposition in the brains of study participants at baseline and follow-up analyses.
2. Though not associated with the cross-sectional extent of β-Amyloid deposition, increased measures of central arterial stiffness were found to be associated with a greater longitudinal accumulation of β-Amyloid in the brains of study participants.
Evidence Rating Level: 2 (Good)
Study Rundown: Hypertension is a well-established risk factor for cognitive impairment and Alzheimer’s disease. Recent evidence indicates that arterial stiffness specifically plays a major role in linking hypertension with its associated pathological features in the brain. In an effort to better characterize this relationship, this longitudinal observational study examined the association between arterial stiffness in different vascular beds and changes in β-Amyloid (Aβ) over time. PET scans were used to assess Aβ deposition during baseline and follow-up periods. At baseline, pulse wave velocity (PWV), a marker of arterial stiffness, was measured in central, peripheral, and mixed vascular beds.
The study found that participants with greater brachial-ankle (mixed vascular bed) PWV were more likely to be Aβ-positive at baseline and follow-up. However, this measurement was not significantly associated with a longitudinal accumulation of Aβ in the brains of participants. Rather, central arterial stiffness was the only factor associated with an increase in Aβ deposition over time. Though providing evidence that vascular disease may contribute to progressive Aβ deposition, this study had a limited sample size, utilized qualitative classification of Aβ-positive participants, and only assessed arterial stiffness at a single point in time.
In-Depth [prospective cohort]: This study examined nondemented participants from the Gingko Evaluation of Memory Study. 91 of these participants received a baseline PET scan to assess Aβ deposition and had their arterial stiffness measured. The mean time to follow-up was 1.8 years. At the follow-up assessment, 81 of these patients remained nondemented and returned for a repeat PET scan. These participants were similar to non-returning participants in baseline characteristics.
Using standardized classification techniques, 48% of participants were Aβ-positive at baseline, while 75% were Aβ-positive upon follow-up. At follow-up, several PWV measurements in different vasculature beds were significantly associated with continuous measures of Aβ deposition, including brachial-ankle PWV (r = 0.32, p < 0. 001). Each 1-SD increase in brachial-ankle PWV was associated with a 4.06-fold increase in the odds of being Aβ-positive (95% CI = 1.83 – 9.06). Changes in the amount of Aβ deposition over time were not correlated with baseline levels of Aβ nor brachial-ankle PWV. However, accumulation of Aβ was linked to greater measures of central arterial stiffness, and when adjusting for covariates a 1-SD increase in carotid-femoral PWV was associated with a nearly 2-fold increase in Aβ deposition over 2 years of follow-up (β = 0.60, p = 0.001).
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