Elderly people suffering from hardening of the arteries are more likely to have beta-amyloid plaques in the brain – an indication of Alzheimer’s disease, according to a study published in the journal Neurology.
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This process is more common when a person ages, but those with Alzheimer’s disease have more of the plaques within particular brain regions, compared with those who do not have the disease.
For the study, researchers from the University of Pittsburgh scanned the brains of 91 participants with an average age of 87, who did not suffer from any form of dementia.
The research team analyzed whether any plaques were present in the participants’ brains, and the stiffness of the participants’ arteries were measured around 2 years later.
Approximately half of all participants had beta-amyloid plaques. The researchers found that these participants were more likely to have high systolic blood pressure and higher average blood pressure, compared with those who did not have these plaques present.
Using the ankle-brachial index method – a test that identifies arterial insufficiency within a limb – the researchers found that participants with beta-amyloid plaques also demonstrated higher arterial stiffness.
Furthermore, for every increase in ankle-brachial arterial stiffness, it was found that the participants were twice as likely to have beta-amyloid plaques in their brain.
Those who had both amyloid plaques and white matter hyperintensities in the brain (brain lesions) were the most likely to demonstrate arterial stiffness.
Dr. Timothy M. Hughes of the University of Pittsburgh explained the findings to Medical News Today:
“Using pulse wave velocity (PWV) to measure arterial stiffness, we found that every unit (1 standard deviation) increase in systemic arterial stiffness was associated with a two-fold increase in the likelihood of having amyloid deposition in the brain.”
“Stiffer arteries also increases the likelihood of having both white matter disease and amyloid deposition in the brain.
Every unit increase in systemic and central PWV increases the odds of this ‘double hit’ (high amyloid and high white matter lesions) by 2.79- and 3.83-fold, respectively. These relationships were not only independent of age, gender and body mass index, but also current blood pressure and taking anti-hypertensive medications.”
Dr. Hughes told Medical News Today that further studies are needed to understand whether amyloid deposition in the brain is a cause or result of dementia.
“Studies like this suggest that amyloid deposition in the brain may also be an age-related phenomena in older adults, and modifiable risk factors, such as hypertension and arterial stiffness, may play an important role,” he says.
But he notes that the fact these relationships are independent of anti-hypertensive medication use is important, as it shows the effects of arterial stiffness are independent of current blood pressure. He also says current anti-hypertensive treatment targeting lowering blood pressure has “little-to-no effect” on reversing arterial stiffness.
“Our arteries continue to harden as we age,” Dr. Hughes adds. “Elevated blood pressure accelerates this stiffening. Current research shows that the best way to reduce and reverse arterial stiffness is to target cardiometabolic risk factors, such as obesity and insulin resistance, with physical activity and weight loss.”