Alzheimer's Risk Gene May Damage Brain Decades Before Symptoms Show
Scans indicate even young adults who have the gene have some white-matter deterioration
WEDNESDAY, May 18 (HealthDay News) -- A gene allele that increases the risk of Alzheimer's disease starts to damage the brain 50 years before symptoms of the disease appear, a new study suggests.
An allele is one of two or more forms of a gene.
In 2009, scientists concluded that the clusterin (CLU) gene boosts the chances of Alzheimer's disease by 16 percent, but it wasn't clear how it increased risk.
This new study concluded that the C-allele of the CLU gene impairs development of myelin, the protective covering around the axons of neurons in the brain. This impairs brain wiring and can make a person more vulnerable to the onset of Alzheimer's later in life.
About 88 percent of whites have the CLU C-allele, according to the University of California, Los Angeles (UCLA) researchers.
For this study, they used a newer type of MRI to map the connections in the brains of nearly 400 healthy adults aged 20 to 30. The scans revealed that participants with the CLU C-allele had lower white matter integrity than those with a different variant called the CLU T-allele.
The findings are interesting on several levels, according to senior study author Paul Thompson, a professor of neurology.
"For example, Alzheimer's has traditionally been considered a disease marked by neuronal cell loss and widespread gray matter atrophy," he said in a UCLA news release. "But degeneration of the myelin in white matter fiber pathways is more and more being considered a key disease component and another possible pathway to the disease, and this discovery supports that."
Understanding the effects of the CLU C-allele could lead to ways to intervene and protect the brain in the decades before Alzheimer's develops, Thompson suggested.
The study appears in the current online edition of the Journal of Neuroscience.
The U.S. National Institute of Neurological Disorders and Stroke has more about Alzheimer's disease.Robert Preidt SOURCE: University of California, Los Angeles, news release, May 2011 Related Articles
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