Finding could point to new targets for treatment, prevention
MONDAY, Feb. 18, 2013 (HealthDay News) -- Damage to tiny blood vessels in the brain might be a secondary contributor to Alzheimer's disease, a new, small study suggests.
Areas of this blood vessel damage, called white matter hyperintensities, are found in the brains of patients with Alzheimer's disease and appear to raise the risk for the condition, the researchers report. It is believed that the accumulation of beta amyloid plaques in the brain are a primary factor in the development of the memory-robbing condition.
"If you have both these white matter hyperintensities and amyloid in the brain, then you are more likely to get Alzheimer's disease down the road than if you just have one of these," said study senior author Adam Brickman, an assistant professor of neuropsychology at Columbia University's Taub Institute for Research on Alzheimer's Disease and the Aging Brain.
The exact connection between this vessel damage and Alzheimer's disease isn't exactly clear, he added. While the study showed an association between the two, it did not prove a cause-and-effect relationship.
"There are a number of things that happen through aging that can influence the vessels of the brain, but there also might be an interaction with Alzheimer's disease itself, where the disease is damaging the vessels or the vessel damage is causing the Alzheimer's disease," Brickman explained.
These tiny vessels might also become damaged through a variety of conditions, including high blood pressure, low blood pressure, oxidative stress, diabetes or inflammation, he explained.
The goal of the research is to one day target these damaged vessels as a way to slow or prevent Alzheimer's disease, Brickman said.
"Maybe not a primary target, but certainly a potential target," he said. "If we know what the risk factors for white matter disease are, they are perfectly reasonable targets for either prevention or possible treatment."
Limiting the damage to the brain's blood vessels is also important, Brickman said. Keeping body weight and blood pressure levels in the normal range and not smoking can go a long way in preventing Alzheimer's disease, he said.
For the study, Brickman's team looked for blood vessel damage in the brains of 20 patients diagnosed with Alzheimer's disease and in 21 people without the condition.
The researchers found that people with Alzheimer's disease had larger areas of damage than those who were not diagnosed with Alzheimer's.
In addition, blood vessel damage in 59 people with mild memory problems who were included in the study were signs that they were at risk for Alzheimer's disease, the researchers added.
Brickman noted that these areas of blood vessel damage are seen in most patients with Alzheimer's disease. "I think the reason we don't see it in every patient is because the MRI technology we use might not be sensitive enough to pick up all the changes in white matter disease," he said.
The report was published in the Feb. 18 online edition of JAMA Neurology.
One expert said the damage to the tiny blood vessels is yet another aspect to the development of Alzheimer's disease, but it complicates understanding the condition.
"This study provides clear evidence that dementia patients in the real world are more complex than those with the pristine pure Alzheimer's disease that we select in research centers," said Dr. Sam Gandy, associate director of the Mount Sinai Alzheimer's Disease Research Center in New York City.
The causes of this blood vessel damage in the brain aren't well understood, but it appears that these white matter hyperintensities do signal brain damage linked to dementia, he said.
Gandy also noted these areas of blood vessel damage make it harder to evaluate the effectiveness of drugs being tested to reduce plaque in Alzheimer's patients.
For more information on Alzheimer's disease, visit the Alzheimer's Association (http://www.alz.org/ ).
SOURCES: Adam Brickman, Ph.D., assistant professor, neuropsychology, Taub Institute for Research on Alzheimer's Disease and the Aging Brain, Columbia University, New York City; Sam Gandy, M.D., associate director, Mount Sinai Alzheimer's Disease Research Center, New York City; Feb. 18, 2013, JAMA Neurology, online