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Can high blood pressure protect the over-80s from dementia?

Updated Thursday, 13 April 2017
New research apparently contradicts what we thought we knew about blood pressure and dementia. Cheryl Hawkes explains why we might all want to stick in the Goldilocks Zone.

It is well known that high blood pressure is a risk factor for dementia, so the results of a new study from the University of California, Irvine, are quite surprising. The researchers found that people who developed high blood pressure between the ages of 80-89 are less likely to develop Alzheimer’s disease (the most common form of dementia) over the next three years than people of the same age with normal blood pressure.

Blood pressure is an approximate measure of how hard the heart has to work to pump blood around the body. As blood pressure increases, so too does the effort of the heart. Over time, the added strain caused by high blood pressure can damage the heart and increase the risk of having a heart attack. High blood pressure can also indicate that the blood vessels are themselves damaged or blocked. This is particularly bad for the brain, because it needs a lot of energy and is highly dependent on a constant supply of oxygen and nutrients that are carried by the blood. In extreme cases, a lack of blood supply in the brain can result in a stroke and vascular dementia.

Damage to blood vessels in the brain is also implicated in the development of Alzheimer’s disease. In addition to delivering oxygen and nutrients, the blood vessels in the brain also act to remove waste products, such as the β-amyloid protein, from the brain. Dysfunction of the vessels can lead to an accumulation of β-amyloid and other toxic proteins in the brain, ultimately leading to death of brain cells and dementia.

It is thought that having high blood pressure increases the risk of developing Alzheimer’s disease. Several long-term studies that have followed people from middle to old age have found that people who have high blood pressure in their 40s and 50s are more likely to develop Alzheimer’s disease in old age compared with those who have normal blood pressure in midlife. Although the definitive reasons for this increased susceptibility are not known, they may relate to damage to the structure of the blood vessels, decreased blood flow to the brain and impaired clearance of toxins from the brain.

However, this latest study from UC Irvine, suggests that having high blood pressure – at least at a certain age – actually protects some people from developing Alzheimer’s disease.

So, how can these apparently contradictory findings be reconciled? The answer may relate to how blood pressure changes normally across the lifespan. As we age, our bodies become less able to compensate for fluctuations in blood pressure, such as when standing from a sitting position.

About 30% of people over 70 years of age experience a feeling of dizziness, light-headedness or weakness when going from sitting to standing (termed postural hypotension). This occurs because of a drop in the amount of blood getting to the brain. In fact, postural hypotension is itself associated with increased risk of developing Alzheimer’s disease. So, people who develop hypertension in late life may do so to compensate for an age-related decrease in blood pressure. This may help them maintain an adequate blood flow to the brain, facilitate waste removal and ultimately protect the brain cells. Alternatively, in people who do not develop Alzheimer’s disease until 90 years of age, or older, changes in blood pressure may occur alongside the onset of dementia, rather than contribute to disease onset.

Increasingly, research points to a role for blood vessels and factors that affect the health of the blood vessels in Alzheimer’s disease. Based on the current understanding, maintaining blood pressure within the “Goldilocks range” – not too high, not too low – is still the best course of action for reducing the risk of developing Alzheimer’s disease.The Conversation

This article was originally published on The Conversation. Read the original article.

 

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