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  • Past studies show there are ways that people can potentially lower their risk of developing Alzheimer’s disease.
  • One main way is by making healthy lifestyle choices, such as limiting alcohol use.
  • A new study has found more evidence suggesting chronic heavy alcohol use may speed up the biological pathways linked to brain aging and Alzheimer’s disease, via an animal model.

While we currently have no cure for the type of dementia known as Alzheimer’s disease, past studies show there are ways that people can potentially lower their risk of developing the condition.

One main way is by making healthy lifestyle choices, such as eating a brain-healthy diet, being physically active, not smoking, getting enough sleep, staying socially connected, and limiting alcohol use.

“Although aging remains the greatest risk factor for Alzheimer’s disease, lifestyle choices can also have a major influence on brain health,” Nagalakshmi (Lakshmi) Balasubramanian, PhD, NIH NIAAA K99/R00 Awardee and postdoctoral fellow in the Department of Cellular and Systems Pharmacology in the College of Pharmacy at the University of Florida, told Medical News Today. “By understanding how factors such as alcohol use, diet, exercise, and sleep affect the aging brain, we may be able to identify opportunities for prevention and develop strategies that help people maintain cognitive health later in life.”

Balasubramanian is the lead author of a new study presented at the 49th annual scientific meeting of the Research Society on Alcohol (RSA) that has found more evidence suggesting chronic heavy alcohol use may speed up the biological pathways linked to brain aging and Alzheimer’s disease, via an animal model.

The findings from the study are yet to be published in a peer-reviewed journal.

For this study, researchers use a mouse model to examine how chronic heavy alcohol use might impact a person’s Alzheimer’s disease risk.

“Heavy alcohol use is a common but often overlooked factor that may affect long-term brain health,” Balasubramanian explained. “Growing evidence suggests that chronic alcohol exposure can accelerate biological aging and trigger processes linked to Alzheimer’s disease, including inflammation, metabolic dysfunction, and the abnormal accumulation of tau protein.”

“Alcohol use can also contribute to depression, anxiety, and social withdrawal — symptoms that are often observed in the early stages of Alzheimer’s disease, sometimes even before noticeable memory problems emerge,” she continued.

“We wanted to better understand the biological mechanisms connecting alcohol use to neurodegeneration and determine why some individuals may be more vulnerable than others to these harmful effects.”
— Nagalakshmi (Lakshmi) Balasubramanian, PhD

Balasubramanian and her team used a mouse model of the ALDH2*2 genetic variant for their research.

“ALDH2 is an enzyme that helps the body remove acetaldehyde, a toxic chemical produced when alcohol is broken down,” Balasubramanian detailed. “People who carry the ALDH2*2 genetic variant have a less efficient version of this enzyme, which allows acetaldehyde to accumulate in the body. This variant is commonly associated with facial flushing after drinking alcohol, but it may also have broader effects on health.”

At the study’s conclusion, researchers found via their animal model that acetaldehyde reshapes the brain at the molecular level and contributes to the development of Alzheimer’s disease.

“One of the most interesting findings from our study was that alcohol-related Alzheimer’s-like pathology appeared to develop differently in males and females,” Balasubramanian said. ”We observed differences in where tau pathology accumulated and which brain cell types were affected. These findings suggest that the biological consequences of alcohol metabolism may not be the same for everyone and that sex-specific factors could influence disease vulnerability.”

“We are now conducting additional studies to better understand the metabolic and molecular mechanisms that drive these differences and how acetaldehyde may contribute to Alzheimer’s-related brain changes,” she added.

MNT spoke with Swapnil Patel, MD, MHCM, FACP, vice chair of the Department of Medicine at Hackensack Meridian Jersey Shore University Medical Center, and assistant professor at Hackensack Meridian School of Medicine in New Jersey — who was not involved in this study — about this research.

Patel commented that this study highlights something doctors are seeing more and more in medicine: heavy alcohol use can increase the risk of brain damage and dementia, including Alzheimer’s disease.

“What makes this research especially interesting is that it helps explain why this happens,” he continued. “As a physician, this reinforces the importance of talking with patients about alcohol use as part of brain health. While we often focus on factors like blood pressure, diabetes, and exercise, alcohol consumption is another lifestyle factor that can significantly affect long-term cognitive health.”

Patel said that the good news is that alcohol use is a risk factor that, unlike genetics, people can modify to potentially lower their risk.

“Researchers estimate that nearly half of dementia cases may be linked to risk factors that can be prevented or improved, and excessive alcohol use is one of them,” he added. “Understanding exactly how alcohol affects the brain can help physicians provide clearer guidance to patients.”

MNT also spoke with Dung Trinh, MD, an internist with MemorialCare Medical Group and the chief medical officer of the Healthy Brain Clinic in Irvine, CA, about this study.

Trinh, who was not involved in this research, said for readers to be careful not to overstate these findings.

“This is preclinical research using a mouse model, so it does not prove that alcohol directly causes Alzheimer’s disease in humans,” he explained. “But it does add to the growing body of evidence suggesting that chronic heavy alcohol use may accelerate biological stress on the brain, especially in people who may already be vulnerable.”

For the next steps in this research, Trinh said the first step should be translating these findings into human studies.

“We need longitudinal research following people over time to understand whether chronic heavy alcohol exposure is associated with measurable Alzheimer’s-related biomarker changes, such as amyloid, tau, neuroinflammation, neurodegeneration, or blood-based biomarker patterns,” he detailed. “Second, I would like to see researchers examine whether certain populations are more vulnerable.”

“Third, we need to understand whether reducing alcohol exposure can meaningfully change brain-health trajectories,” Trinh added. “In other words, can cutting back or stopping heavy alcohol use reduce inflammatory or neurodegenerative markers over time? That would be extremely valuable for prevention counseling.”

“This study raises an important question around the ALDH2*2 variant, which may impair the body’s ability to clear acetaldehyde efficiently. If some individuals accumulate more toxic alcohol byproducts than others, that could have implications for personalized risk assessment.”
— Dung Trinh, MD