Alzheimer s linked to immune-gene mutation

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It s an odd coincidence that s good news for Alzheimer s research. Two groups of researchers using vastly different approaches have independently identified a genetic mutation that increases one s odds of developing the brain disease and perhaps foreshadows how drugs could one day be used to stave it off.

People with the gene called TREM2 have a three- to fivefold increased chance of developing Alzheimer s, apparently because their body s white blood cells are impaired in their ability to devour a plaque-like protein called beta amyloid, which builds up in between the nerve cells of the brain and appears to play an important role in causing Alzheimer s.

In one study researchers led by Dr. Kari Stefansson of deCODE Genetics in Iceland studied the genomes of 2,261 Icelanders, trying to find some pattern that might be used to discriminate people admitted to nursing homes before age 75 from those who were still living at home at 85. They zeroed in on TREM2.

In the other study, researchers with University College London and the National Institute on Aging asked scientists around the world with genetic data from Alzheimer s patients to look for TREM2 mutations. They found it occurred in 1 to 2 percent of patients, compared to one-half of 1 percent of people in the general population. Both studies are published in the New England Journal of Medicine.

ACSH s Dr. Gilbert Ross says these findings might one day lead to the development of a drug that could treat Alzheimer s. If this genetic mutation discovery is confirmed, a whole range of treatments to augment immune response and enhance the body s ability to gobble up amyloid plaques may prove beneficial. Unfortunately, such a drug still seems like a long way off, he says.