May 18, 2011 -- Young adults who carry a so-called Alzheimer's risk gene show disruption in their brains as early as their 20s, according to new research.
Researchers from the University of California, Los Angeles used a special MRI scan that maps brain connections to examine 398 healthy young adults. Some carried the variant of the gene linked with Alzheimer's risk and some did not.
"The people who carry this gene have severely impaired wiring in most of their brain, even when they are young," says researcher Paul M. Thompson, PhD, professor of neurology at the University of California, Los Angeles David Geffen School of Medicine.
Even so, they don't notice symptoms of Alzheimer's disease, such as memory loss at this time, he tells WebMD. Following a healthy lifestyle early can offset the genetic risk, he says.
The study is published in The Journal of Neuroscience.
For late-onset Alzheimer's disease, which appears in old age, scientists know there is a strong genetic link.
In 1993, scientists discovered the gene known as ApoE4, carried by about 25% of people. It triples the risk of Alzheimer's disease.
Then, in 2009, scientists found more ''risk'' genes. One is called clusterin or CLU. Those who have the CLU gene form known as CLU-C have about a 16% higher risk of Alzheimer's disease than those who have the CLU-T gene form.
However, the experts who discovered the new risk gene could not say why it boosted the risk. "This is the first clear evidence of what it does," Thompson tells WebMD.
About 88% of whites carry the CLU-C variant, Thompson says.
He used a special MRI scan to look closely at the brain's connections. Among the 398 people scanned, some had one copy of the CLU-C variant, some had two, and some had none.
"We basically wanted to see how the people who carry this gene differ," Thompson tells WebMD.
They found the CLU-C carriers had what scientists call lower ''fractional anisotropy." This is a measure of white matter brain tissue integrity. ''The white matter integrity was about 10% lower in the carriers of the gene compared to the ones who didn't have it," he says. Those who carried two copies of CLU-C had even lower white matter integrity, he says.
The findings suggested that the change in the white matter was due to reduced integrity of the myelin, the protective coating covering the brain cells.
The study suggests the gene variant ''does its work very early," Thompson says. And it does so, he says, not by forming the plaques associated with Alzheimer's disease but by damaging the myelin, the protective coating on the brain's nerve cells.
It's known that in Alzheimer's disease, the white matter pathways deteriorate due to impaired myelin and other factors.