The gene responsible for “Asian glow,” a condition in which a person's face flushes red after drinking alcohol, has been linked to a faster progression of Alzheimer's disease, according to a study released this month by researchers at Stanford.

Individuals who have a defective version of an enzyme that metabolizes alcohol can experience an increased buildup of toxins, which can lead to cell damage and has been linked to accelerated development of Alzheimer's, the researchers found.

The body converts alcohol into a toxin that can damage DNA before processing it into an energy source. But approximately 560 million individuals of East Asian descent carry a mutated version of the enzyme that’s ineffective at breaking down that toxin. The defective gene is also associated with higher incidences of esophageal cancer, heart attacks and osteoporosis.

Findings from the study, published last Thursday in the journal Acta Neuropathologica Communications, suggest that alcohol increases injury to brain cells, accelerates signs of Alzheimer's in animals and increases cell damage in patients with the disease.

“The science means that it is a bad idea if you have this mutation and have a family history of Alzheimer’s disease to drink excessively,” Daria Mochly-Rosen, senior author of the study and a professor of chemical and systems biology at Stanford, said.

Researchers studied genetically engineered mice with the mutated gene and injected them with an amount of alcohol equivalent to about two drinks per day in humans every day for 11 weeks. They also examined cell cultures from individuals with Alzheimer's disease.

In both cases, they found that the mice and cell cultures with the mutated gene had more free radicals, which form toxic compounds, according to a news release from Stanford Medicine. The body normally eliminates those compounds, but when they accumulate in people who have the defective gene, they damage structures in cells containing the enzyme responsible for getting rid of them.

Mochly-Rosen said it's the damage of these structures that is linked to an accelerated progression of Alzheimer's.

Authors of the study also found that a drug can reduce the risk of Alzheimer's by correcting the defective gene, Mochly-Rosen added.

Dr. Ronald Petersen, director of the Mayo Clinic Alzheimer’s Disease Research Center, who was not involved with the study, said the new research may shed light on the complex relationship between alcohol consumption and cognitive aging. He noted, however, that while findings of a potential treatment for the mutated gene are exciting, caution needs to be expressed since the study involved mice and cultured cells.

“Given the frequency of this mutation, approximately 8 percent of the population, and its frequency in the Eastern Asian population, it is important to understand potential mechanisms,” Petersen said in an email. “Larger scale epidemiological studies supporting the role of the mutation more widely would lend enthusiasm for pursuing human clinical trials in the future.”

About 50 million people worldwide live with dementia — a group of diseases and conditions characterized by memory loss that includes Alzheimer's — and that number is expected to nearly triple by 2050, according to the World Health Organization.

In the United States, up to 5 million people have the disease, according to the Alzheimer's Association. It is the sixth leading cause of death in the country.

Mochly-Rosen said she hopes the published findings will trigger a potential clinical study that will look into changing the recommendation of alcohol use in people who have Alzheimer's.

“If we show in a clinical study that indeed there is an acceleration of the disease, then if someone has symptoms of the disease or a family member with it, their physician will be in a position to recommend not drinking alcohol,” she said. “Human studies are needed before making this recommendation.”