Brain scan study confirms role of Alzheimer’s genes
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A study of brain scans has confirmed the role of several genes linked with Alzheimer’s disease, and turned up two others that are worth exploring, U.S. researchers said on Monday.
A team at Massachusetts General Hospital in Boston used magnetic resonance imaging or MRI scans to study changes in brain structures—such as the size of the hippocampus and amygdala—in 700 healthy volunteers and Alzheimer’s patients.
They used computer programs to sort through the genetic sequences of the 700 volunteers to see which gene mutations are most linked with these changes.
The study turned up a known offender - the APOE4 gene - as the most strongly linked with the disease, but it also confirmed three other genes - CLU, CRI, PICALM - that have been more recently linked with Alzheimer’s.
And they fingered two others - BIN1 and CNTN5 - which have been suspected, but not strongly linked with Alzheimer’s.
While the findings are preliminary, “they may help prioritize targets for future genetic studies,” Drs. Alessandro Biffi and Christopher Anderson of Massachusetts General and the Broad Institute wrote in the Archives of Neurology.
Researchers suspect genes can explain 60 to 80 percent of the risk of late onset Alzheimer’s disease, the kind that occurs with age.
Scientists have long understood the genetic cause of early onset Alzheimer’s, a rare type that affects people under 60, but finding genes that explain the more common late onset form has been far more challenging.
Paul Thompson of the University of California Los Angeles Laboratory of Neuro Imaging, who was not involved with the study, said the findings offer new way of confirming the role of genes in Alzheimer’s disease.
He said it now appears unlikely that there are many more single genes like APOE4 that contribute significantly to Alzheimer’s disease, but there are likely many genes that, when combined, raise a person’s risk.
“The way most of us will get Alzheimer’s is through these big sets of risk genes. They are beginning to discover a few of them. None of them is sufficient to get Alzheimer’s on its own,” Thompson said in a telephone interview.
“It’s the slow erosion of the brain from an army of culprits.”
Thompson said understanding the role of even a few of these genes will help drug companies devise better weapons to fight Alzheimer’s.
Current drugs help manage symptoms but, so far, no treatment can stop the progression of Alzheimer’s, which can start with vague memory loss and confusion before progressing to complete disability and death.
The U.S. government, private insurance and individuals spend $172 billion a year to care for people with Alzheimer’s disease, the most common cause of dementia that affects 26 million people globally.
SOURCE: Archives of Neurology, June 14, 2010.
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