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Alzheimer's damage may begin at a young age, study finds

May 12, 2011|By Shari Roan, Los Angeles Times / For the Booster Shots blog
  • New findings suggest that changes in myelin, which protects nerve cells, may be a sign of increased risk of developing Alzheimer's later in life.
New findings suggest that changes in myelin, which protects nerve cells,… (Kali Ciesemier / For the…)

Alzheimer's disease research has shifted to looking for the earliest signs and symptoms of the disease process. A new study has found evidence of  early brain damage in some young people at increased risk for the disease.

Researchers led by Dr. Paul Thompson, a UCLA professor of neurology, conducted brain scans on 398 young, healthy people ages 20 to 30. Those participants who carried a particular gene mutation that is known to raise the risk of Alzheimer's -- linked to the CLU gene -- had unique characteristics in white matter (the bundles of nerve cells) in multiple brain regions, including in some areas known to become damaged in Alzheimer's disease. The findings suggest that changes in myelin, the substance that protects nerve cells, may be a sign of increased risk of developing the disease later in life.
 
"Alzheimer's has traditionally been considered a disease marked by neuronal cell loss and widespread gray matter atrophy," Thompson said in a news release. "But degeneration of 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."

People who have this particular mutation in the CLU -- which is common -- aren't doomed to develop Alzheimer's disease, the authors noted. And young people who have these changes in white matter are not cognitively impaired. But knowledge about this genetic risk could be used to help prevent the disease later in life, the authors said.

The study was published online last week in the Journal of Neuroscience.

Related:

Broader definition of Alzheimer's could help doctors diagnose it earlier

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