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Original Investigation |

Arterial Stiffness and β-Amyloid Progression in Nondemented Elderly Adults

Timothy M. Hughes, PhD, MPH1; Lewis H. Kuller, MD, DrPH2; Emma J. M. Barinas-Mitchell, PhD2; Eric M. McDade, DO3; William E. Klunk, MD, PhD4; Ann D. Cohen, PhD4; Chester A. Mathis, PhD5; Steven T. DeKosky, MD6; Julie C. Price, PhD5; Oscar L. Lopez, MD3
[+] Author Affiliations
1Department of Internal Medicine, Wake Forest School of Medicine, Wake Forest University, Winston-Salem, North Carolina
2Department of Epidemiology, Graduate School of Public Health, University of Pittsburgh, Pittsburgh, Pennsylvania
3Department of Neurology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania
4Department of Psychiatry, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania
5Department of Radiology, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania
6Department of Neurology, School of Medicine, University of Virginia, Charlottesville
JAMA Neurol. 2014;71(5):562-568. doi:10.1001/jamaneurol.2014.186.
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Importance  Recent studies show that cerebral β-amyloid (Aβ) deposition is associated with blood pressure and measures of arterial stiffness in nondemented individuals.

Objective  To examine the association between measures of arterial stiffness and change in Aβ deposition over time.

Design, Setting, and Participants  Deposition of Aβ was determined in a longitudinal observational study of aging by positron emission tomography using the Pittsburgh compound B twice 2 years apart in 81 nondemented individuals 83 years and older. Arterial stiffness was measured with a noninvasive and automated waveform analyzer at the time closest to the second positron emission tomography scan. All measures were performed under standardized conditions. Pulse wave velocity (PWV) was measured in the central (carotid-femoral and heart-femoral PWV), peripheral (femoral-ankle PWV), and mixed (brachial-ankle PWV) vascular beds.

Main Outcomes and Measures  The change in Aβ deposition over 2 years was calculated from the 81 individuals with repeat Aβ–positron emission tomography.

Results  The proportion of Aβ-positive individuals increased from 48% at baseline to 75% at follow-up. Brachial-ankle PWV was significantly higher among Aβ-positive participants at baseline and follow-up. Femoral-ankle PWV was only higher among Aβ-positive participants at follow-up. Measures of central stiffness and blood pressure were not associated with Aβ status at baseline or follow-up, but central stiffness was associated with a change in Aβ deposition over time. Each standard deviation increase in central stiffness (carotid-femoral PWV, P = .001; heart-femoral PWV, P = .004) was linked with increases in Aβ deposition over 2 years.

Conclusions and Relevance  This study showed that Aβ deposition increases with age in nondemented individuals and that arterial stiffness is strongly associated with the progressive deposition of Aβ in the brain, especially in this age group. The association between Aβ deposition changes over time and generalized arterial stiffness indicated a relationship between the severity of subclinical vascular disease and progressive cerebral Aβ deposition.

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Figure.
A Conceptualized Trajectory of Vascular Factors Related to Arterial Stiffness and β-Amyloid Deposition in the Brain Across Adulthood

Figure represents the proposed relationships between factors related to arterial stiffness and age. Arterial stiffness is measured by blood pressure and pulse wave velocity. Joas et al23 and others24,25 show that blood pressure begins to decline late in life, at least partly explaining why midlife blood pressure is a risk factor for dementia and late-life measures are not. In contrast, pulse wave velocity, a surrogate measure for arterial stiffness, does not appear to decline in late life and continues to increase with age.21,26 A recent prospective study of β-amyloid deposition suggests that its progression occurs in a protracted manner over several decades before the diagnosis of dementia.27 Interestingly, these data also suggest that the rate of β-amyloid deposition slows and may level off as deposition approaches a saturation point.

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