Early Plaque Build-Up May Signal Alzheimer’s Disease

April 4, 2012

Alzheimer’s is characterized by the buildup of beta-amyloid, a protein that accumulates in the brains of those with the disease. But at least 20 percent of elderly men and women also have evidence of beta-amyloid buildup in the brain on autopsy, despite having normal memory and thinking skills while alive.

Now researchers have demonstrated that plaque buildup occurs in many well-functioning people beginning in middle age or even earlier, and are correlated with subtle disturbances in memory. The findings, published in the journal Neurology, provide further evidence that Alzheimer’s is a long process that begins well before the telltale memory loss and other symptoms of the disease become apparent.

For the study, researchers at the University of Texas at Dallas and UT Southwestern Medical Center recruited 137 healthy men and women ranging in age from 30 to 89. All were free of obvious memory problems.

The study participants underwent brain scans using special dyes to look for signs of beta-amyloid buildup. They also were given tests to look for subtle signs of memory and thinking problems, even though their memory showed no obvious signs of failing.

The researchers found that the older someone was, the more beta-amyloid they tended to have. “In our study, we observed that even in adults with apparently good cognitive health, increasing amounts of beta-amyloid in the brain are related to subtle changes in memory and mental function,” said study author Denise C. Park of the Center for Vital Longevity at the University of Texas at Dallas.

Plaque buildup was notably elevated in about one in five of those over 60, more commonly in those who carried a gene called APOE-E4 that raises the risk of developing Alzheimer’s disease. Those with more plaque tended to score worse on memory tests than their peers with less plaque; they did not process thoughts as quickly and were less able to think logically and solve problems requiring reasoning skills.

“We found that this high-amyloid group showed deficits in cognitive performance, even though the individuals were well educated and scored normally on our standard tests of cognition,” said Dr. Karen Rodriguez, lead author of the study.

“Our findings suggest that subtle effects on cognition occur early,” Dr. Park said. “These are important findings, because imaging patients when they first show signs of very mild cognitive impairment could be essential to determining their risk of future disease.”

Determining who will ultimately develop Alzheimer’s is important, since many researchers believe that the best strategy to treat the disease may be to develop new drugs that can be given during middle age, before brain deterioration from the disease becomes irreparable. Currently available drugs do nothing to stop progression of Alzheimer’s.

“Just as many adults take aspirin to lower their risk of heart disease or stroke, one day we may be able to help protect our brains and cognitive health by starting a treatment in our 40s or 50s,” Dr. Park said.

The authors also found that some people in their 60s, 70s and 80s seemed to defy the brain deterioration of old age. Levels of beta-amyloid buildup in some of these men and women were as low, or lower, than some others in their 30s, 40s or 50s.

“Another avenue of our future work will be to investigate what factors enable these individuals to maintain cognitive health well into old age, whether they be genetic factors, lifestyle factors or environmental issues,” said Dr. Park. “Understanding how the brain and mind stay healthy and vital over the long term will help guide our efforts to delay or even prevent the devastation caused by diseases like Alzheimer’s.”

By ALZinfo.org, The Alzheimer’s Information Site. Reviewed by William J. Netzer, Ph.D., Fisher Center for Alzheimer’s Research Foundation at The Rockefeller University.

K.M. Rodrigue, PhD K.M. Kennedy, PhD M.D. Devous, Sr., PhD, et al: “Beta-Amyloid Burden in Healthy Aging: Regional Distribution and Cognitive Consequences.” Neurology Vol. 78, 2012, pages 387-395.


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