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People with one of two natural variations in certain genes appear to be at much higher risk of developing Alzheimer's disease, researchers report.
The genes make interleukin-1 (IL-1), an inflammation-promoting protein produced by the immune system. There are two different versions of IL-1 -- interleukin-1 alpha (IL-A) and interleukin 1-beta (IL-1B).
"We've known for some time that more interleukin-1 was produced in the brains of people with Alzheimer's disease, but we weren't sure why," Dr. Sue T. Griffin from the Central Arkansas Veterans Healthcare System in Little Rock, told Reuters Health. The finding may explain why some anti-inflammatory drugs have been shown to reduce the risk of Alzheimer's disease, she said.Griffin and her team looked at a specific variation in the gene for IL-1A (IL-1A2). Those people who have two copies of IL-1A2 -- one from each parent -- have three times the risk of the memory-robbing disorder than those with other versions of the gene. Those who have two copies of IL-1A2 in addition to a second variation in IL-1B (IL-1B2) are more than 10 times as likely to have Alzheimer's disease, according to the report in the March issue of the Annals of Neurology.
The researchers compared the genetic makeup of 232 people with Alzheimer's disease to 167 people without the disease. Overall, 13% of those with Alzheimer's had two copies of IL-1A2 compared with 7% of those without the disease.
A variation in IL-1A also appears to be linked to the development of Alzheimer's disease at an earlier age.
In a second study in the same journal, Griffin, Dr. Luigi Grimaldi from the University of Milan, Italy, and colleagues found that people who had an IL-1A variation were almost five times as likely as others to develop Alzheimer's before the age of 65 years. Those with an IL-1B variation had nearly double the risk of developing the disease early on.
Overall, people with the IL-1A variation developed Alzheimer's 9 years earlier than people with other forms of the gene.
The researchers looked at the IL-1 genes in 318 Alzheimer's patients and 335 people without the disease.
"These results clearly demonstrate an association of (certain IL-1 genes) with Alzheimer's disease," Griffin said. "Armed with this information, we can work toward treatments that prevent Alzheimer's disease or treat it once it occurs."SOURCE: Annals of Neurology 2000;47:361-365, 365-368."This also helps to explain why earlier studies showed that anti-inflammatory drugs delay the onset of Alzheimer's disease in some patients," she added. "We need to do more studies to determine how anti-inflammatory drugs might best be used to prevent Alzheimer's disease."
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