Even modest drinking can speed up the loss of brain cells and formation of the plaques that are a hallmark of Alzheimer's disease, research in mice shows.

These plaques are an accumulation of toxic proteins.

"These findings suggest alcohol might accelerate the pathological cascade of Alzheimer's disease in its early stages," said study co-author Shannon Macauley. She is an associate professor of physiology and pharmacology at Wake Forest University School of Medicine in Winston-Salem, N.C.

About 60% to 80% of dementia cases are Alzheimer's disease, according to the Alzheimer's Association.

For the new study, researchers used a 10-week chronic drinking approach where mice were given the choice to drink water or alcohol. This mimics human behavior regarding alcohol consumption.

The investigators then explored how voluntary, moderate consumption of alcohol affected healthy brain function and behavior. They also looked at whether it altered the disease path associated with the early stages of Alzheimer's.

The study found increases in brain atrophy (the loss of brain cells) and an increased number of amyloid plaques, including a greater number of smaller plaques. This potentially would set someone up for increased plaque proliferation in later life.

In addition, the findings showed that acute withdrawal of alcohol increased levels of amyloid-beta, a key component of amyloid plaques that accumulate in Alzheimer's.

Macauley had previously shown that elevated blood sugar increased amyloid-beta and amyloid plaques.

In this study, the researchers found that even moderate drinking caused elevations in blood sugar and markers of insulin resistance. This increases the risk of type 2 diabetes, as well as heart and vascular disease, in addition to Alzheimer's disease.

Moderate alcohol use also altered anxiety and dementia-related behaviors.

"These preclinical findings suggest that even moderate consumption of alcohol can result in brain injury," Macauley said in a university news release. "Alcohol consumption may be a modifiable risk factor for Alzheimer's disease and dementia."

However, animal research often yields different results in humans.

The findings were published in the February issue of Neurobiology of Disease.

The study was a collaboration with Jeffrey Weiner, professor of physiology and pharmacology at Wake Forest through the medical school's Alzheimer's Disease Research Center and Translational Alcohol Research Center.