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Think Twice Before That Next Drink: Alcohol’s Shocking Link to Alzheimer’s

A study by Wake Forest University School of Medicine found that even modest alcohol consumption can expedite brain atrophy and amplify the formation of amyloid plaques, which are linked to Alzheimer’s disease. Using mouse models, researchers discovered that consistent alcohol exposure disrupted metabolism and raised blood sugar levels, increasing risks for other ailments, including type 2 diabetes and cardiovascular diseases.

A research study suggests that even modest alcohol consumption can hasten brain degeneration and amplify amyloid plaque formation, intensifying Alzheimer’sAlzheimer's disease is a disease that attacks the brain, causing a decline in mental ability that worsens over time. It is the most common form of dementia and accounts for 60 to 80 percent of dementia cases. There is no current cure for Alzheimer's disease, but there are medications that can help ease the symptoms.” data-gt-translate-attributes=”[{“attribute”:”data-cmtooltip”, “format”:”html”}]”>Alzheimer’s disease risks.

Alzheimer’s disease is the most common form of dementia, accounting for 60% to 80% of dementia cases, according to the Alzheimer’s Association. While current research suggests alcohol use disorder is a risk factor in Alzheimer’s disease, the impact alcohol use disorder has on Alzheimer’s disease pathology is an area of continued research.

In a preclinical study, scientists at Wake Forest University School of Medicine showed that even modest amounts of alcohol can accelerate brain atrophy, which is the loss of brain cells, and increase the number of amyloid plaques, which are the accumulation of toxic proteins in Alzheimer’s disease.

The study was published in the journal Neurobiology of Disease.

“These findings suggest alcohol might accelerate the pathological cascade of Alzheimer’s disease in its early stages,” said Shannon Macauley, Ph.D., associate professor of physiology and pharmacology at Wake Forest University School of Medicine.

The study was a collaboration led by Macauley and Jeffrey Weiner, Ph.D., professor of physiology and pharmacology at Wake Forest University School of Medicine, through the medical school’s Alzheimer’s Disease Research Center and Translational Alcohol Research Center.

Research Methodology and Discoveries

Using mouse models of Alzheimer’s disease-related pathology, researchers used a 10-week chronic drinking approach where mice were given the choice to drink water or alcohol, mimicking human behavior regarding alcohol consumption. They then explored how voluntary, moderate consumption of alcohol altered healthy brain function and behavior and whether it altered the pathology associated with the early stages of Alzheimer’s disease.

The researchers found that alcohol increased brain atrophy and caused an increased number of amyloid plaques including a greater number of smaller plaques, potentially setting the stage for increased plaque proliferation in later life.

Interestingly, researchers also noted that acute withdrawal of alcohol increased the levels of amyloid-beta, which is a key component of amyloid plaques that accumulate in Alzheimer’s disease.

Further analysis showed that chronic alcohol exposure poorly regulated brain and peripheral metabolism—another way to accelerate Alzheimer’s disease pathology. Macauley previously demonstrated that elevated blood sugar increases amyloid-beta and amyloid plaques. In the current study, researchers found that even moderate drinking caused elevations in blood sugar and markers of insulinInsulin is a hormone that regulates the level of glucose (sugar) in the blood. It is produced by the pancreas and released into the bloodstream when the level of glucose in the blood rises, such as after a meal. Insulin helps to transport glucose from the bloodstream into the cells, where it can be used for energy or stored for later use. Insulin also helps to regulate the metabolism of fat and protein. In individuals with diabetes, their body doesn't produce enough insulin or doesn't respond properly to insulin, leading to high blood sugar levels, which can lead to serious health problems if left untreated.” data-gt-translate-attributes=”[{“attribute”:”data-cmtooltip”, “format”:”html”}]”>insulin resistance, which increases the risk not only for Alzheimer’s disease but also for other diseases such as type 2 diabetes and cardiovascular diseaseCardiovascular disease refers to a group of conditions that affect the heart and blood vessels, such as coronary artery disease, heart failure, arrhythmias, and stroke. It is caused by a variety of factors, including lifestyle choices (such as smoking and poor diet), genetics, and underlying medical conditions (such as high blood pressure and diabetes). Cardiovascular disease is a leading cause of death worldwide, but can often be prevented or managed through lifestyle changes, medications, and medical procedures such as bypass surgery and angioplasty.” data-gt-translate-attributes=”[{“attribute”:”data-cmtooltip”, “format”:”html”}]”>cardiovascular disease.

Implications of the Study

The study also found that moderate alcohol use altered anxiety and dementia-related behaviors.

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

Reference: “Ethanol exposure alters Alzheimer’s-related pathology, behavior, and metabolism in APP/PS1 mice” by Stephen M. Day, Stephen C. Gironda, Caitlin W. Clarke, J. Andy Snipes, Noelle I. Nicol, Hana Kamran, Warner Vaughan, Jeffrey L. Weiner and Shannon L. Macauley, 16 December 2022, Neurobiology of Disease.
DOI: 10.1016/j.nbd.2022.105967

This study was supported by the National Institute on Alcohol Abuse and Alcoholism Grant No. P50AA026117, National Institute on Aging Grant P30AG072947, National Institute on Aging Grant No. R01AG068330, National Institute on Alcohol Abuse and Alcoholism Grant T32AA007565, National Institute on Aging Grant No. K01AG050719, BrightFocus Foundation Grant No. A20201775S, and grant from the Averill Foundation.

Source: SciTechDaily