Researchers here show an association between blood vessel stiffening and the deposition of β-amyloid in people who have not yet developed Alzheimer's disease. In general we should not be surprised to see associations between different measurable aspects of aging, as aging is a global phenomenon resulting from a small number of root causes. Thus many of the outcomes proceed in parallel to one another.
Here, however, the causes of stiffness and rising levels of amyloid formation are - so far as we know at present - two somewhat independent groups of processes. So the fact that they associate suggests that vascular dysfunction contributes to Alzheimer's disease, a relationship already suspected from a range of other evidence. Certainly the degeneration of blood vessels with aging is the cause of other forms of dementia.
Deposition of Aβ was determined in a longitudinal observational study of aging by positron emission tomography twice 2 years apart in 81 nondemented individuals 83 years and older. Arterial stiffness was measured with a noninvasive and automated waveform analyzer. Pulse wave velocity (PWV) was measured. The change in Aβ deposition over 2 years was calculated with repeat Aβ-positron emission tomography.
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.
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.