Two new studies have identified a specific gene called TREM2 that seems to greatly increase the risk for Alzheimer’s disease and point to the role that inflammation may have in this disease.

The first study out of Iceland sequenced the genomes of 2,251 people who lived in that country. This team identified the TREM2 mutation as being involved in Alzheimer’s disease and then confirmed their findings in genetic samples taken from people who lived in Norway, Netherlands, Germany and the United States.
The second study, which was led by a research team from the United Kingdom and included researchers from the National Institutes of Health and the Mayo Clinic, found the TREM2 mutation in more than 1,000 people who had Alzheimer’s.

“The discovery of the TREM2 mutation helps highlight how important the inflammatory process is in Alzheimer’s, an idea discussed among those in the field for years,” reported Shirley S. Wang in an article in The Wall Street Journal.

This new gene isn’t common, with less than one-half of one percent of the population thought to have it. However, having this gene seems to triple the chances that the person will develop Alzheimer’s disease. This gene also appears to harm memory as well as thinking in older people who do not have dementia.

Dr. Allan Levey, the director of an Alzheimer’s program at Emory University, noted that this gene raises the risk of Alzheimer’s disease by about the same amount as the problem version of the ApoE gene, which previously had been found to have a large impact on the risk of Alzheimer’s. (Approximately 17 percent of the population has at least one copy of the problem ApoE gene, but researchers have determined that approximately half of all people who have Alzheimer’s have the ApoE gene.)

Researchers believe that the TREM2 gene aids the immune system in keeping inflammation in check in the brain through clearing trash away, such as the amyloid plaques that are a hallmark of Alzheimer’s. Scientists have determined that mutations in the genes actually impair these tasks. The researchers’ goal is to develop treatments  that would restore the gene’s function and stop inflammation because they believe that will help stop the disease.

“Genetic mutations that are confirmed as Alzheimer's risk genes tell us more about the disease — often that Alzheimer's is somehow connected to the regular function of the gene,” an Alzheimer’s Association newsletter stated. “And they may become targets for therapies or point us to new targets for therapies.”

This news is important in many ways. First of all, it’s giving researchers new leads to follow as they try to find ways to stop this terrible disease. Secondly, it provides added information about the role that inflammation may play in Alzheimer’s. And because of that, I’d suggest that it also provides added ammunition about what we should be doing In our day-to-day lives to stop inflammation.