Alzheimer’s disease and heart disease are two of the leading causes of death, both affecting millions of people … [+]
Alzheimer’s disease and heart disease are two of the leading causes of death, both affecting millions of people around the world. More and more research has shown that brain and heart health may be more linked than previously thought. At the interface between brain cells and blood vessels, the blood-brain barrier undergoes damage with age that appears to contribute to a decline in cognitive function. In the most recent installment of this series on Alzheimer’s disease, we discussed the role that insulin receptors in the blood-brain barrier may play in the development of Alzheimer’s disease. Here we will delve deeper into the functions of the blood-brain barrier and how we can prolong normal cognitive function in people with Alzheimer’s disease.
As we age, the blood-brain barrier develops small lesions that increase its permeability and impair its function. Emerging research has shown that increased blood-brain barrier dysfunction appears to occur early in the disease course, possibly before neurodegeneration, brain atrophy, and even cognitive symptoms. How this dysfunction contributes to Alzheimer’s disease is not well understood until now. A team from the Medical University of Georgia and collaborating institutions found that small lesions in the brain’s hair-thin microvascular vessels correspond to white matter changes that ultimately contribute to worsening cognitive function and memory impairment.
What is white matter? Unlike gray matter which consists of neural cell bodies, white matter refers to the myelinated or enclosed axon fibers that allow the rapid transmission of nerve impulses. White matter is essential for brain health and carrying out daily functions, including memory, problem solving and coordination. Not surprisingly, clinical observations have shown that changes in the white matter of the brain during Alzheimer’s disease correlate with memory impairment and impaired cognition.
In an earlier report, the team identified a link between white matter deficits and blood-brain barrier dysfunction. It appears that the presence of small lesions in the microvessels of the blood-brain barrier causes oxidative stress and inflammation. Subsequent MRI images indicated that the increased inflammation may contribute to changes in the brain’s white matter.
To determine how blood-brain barrier dysfunction causes white matter changes in Alzheimer’s disease, Bagi et. already examined the brains of 28 people over the age of 65. This cohort included both men and women known to have Alzheimer’s disease, with or without apparent microvascular damage, in addition to healthy controls. They obtained white matter and cerebral vascular samples from the prefrontal cortex, an area of the brain particularly vulnerable to degeneration in Alzheimer’s disease.
In the first study, researchers noted that the brain blood vessels in people diagnosed with Alzheimer’s were significantly affected. These blood vessels did not appear to dilate properly even when exposed to powerful dilation factors. The ability of blood vessels to dilate is critical for controlling blood flow across the blood-brain barrier. Decreased dilation can not only contribute to increased inflammation and oxidative stress, but also puts blood vessels at risk for developing additional lesions.
Bagi et. although they also found that greater damage to microvessels corresponded to more significant changes in white matter. To their surprise, this was accompanied by an increase in the number of specific brain cells called astrocytes. An important part of the blood-brain barrier, these supporting cells regulate the exchange of nutrients and waste between the brain and the blood. Researchers speculate that in progressive microvascular dysfunction in Alzheimer’s disease, astrocytes undergo changes that cause them to become more reactive and inflammatory. The additional damage these cells cause to the brain-brain barrier and nearby cells makes the brain more vulnerable to cognitive changes.
Overall, this study adds to the growing body of evidence that inflammation within the blood-brain barrier causes structural changes in the brain. Fortunately, unlike neurodegeneration, vascular inflammation can be modified through diet and exercise. Dr. Zsolt Bagi, lead author and biologist at the Medical College of Georgia, wrote: “We propose that if you prevent the development of the microvascular component, you can at least add several years of more normal functioning to individuals with Alzheimer’s disease.” Understanding the connection between heart and brain health may one day allow early screening for Alzheimer’s disease and other forms of dementia through routine blood tests.
