Two international teams of scientists have identified a rare mutation in a gene linked with inflammation that significantly increases the risk for the most common form of Alzheimer’s disease, the first such discovery in at least a decade.

The findings, published on Wednesday in the New England Journal of Medicine, offer new insights into the underpinnings of Alzheimer’s, a deadly, brain-wasting disease that robs people of their memories, their independence and their lives.

In separate studies, teams led by privately held deCode Genetics and John Hardy of University College London found that people with a mutation in a gene called TREM2 were four times as likely to have Alzheimer’s as people who did not have the gene.

“It quadruples the risk of Alzheimer’s,” said Dr. Kari Stefansson of Reykjavik-based deCode in a telephone interview.

The level of risk compares with ApoE4, the best-known genetic cause of late-onset Alzheimer’s, the form of the disease that occurs in older adults.

But this new gene variant is 10 times more rare than ApoE4, which is present in about 40 percent of people with late-onset Alzheimer’s.

Rare or not, scientists say the discovery represents a big breakthrough for Alzheimer’s research.

“This is one of the most common, most devastating illnesses in humans and we still don’t have a very good understanding of what causes the disease,” said Dr. Allan Levey, director of the Emory Alzheimer’s Disease Center of Excellence in Atlanta, which helped confirm the deCode findings.

“In my mind, this is very important. It gives us another important clue as to one of the biological factors that contribute to causing the disease,” he said.

Despite numerous costly attempts, drug companies have been stymied in their efforts to develop drugs that can alter the steady course of Alzheimer’s, which affects more than 5 million Americans and costs the United States more than $170 billion annually to treat.

Current research efforts have focused on removing sticky clumps of a protein called beta amyloid that accumulate in the brains of people with Alzheimer’s disease. But several drugs that have been developed to remove these proteins have failed to produce a significant improvement in patients with mild to moderate forms of dementia.