Alcohol abuse may hasten the stream of Alzheimer’s disease.

Alcohol abuse may hasten the stream of Alzheimer’s disease.

According to recent studies conducted by researchers from Scripps Research and the University of Bologna, the occurrence of alcohol use disorder (AUD) in combination with a genetic predisposition may hasten the progression of Alzheimer’s disease.

The study, which was carried out on mice, shows that repeated episodes of alcohol intoxication in rodents with a hereditary propensity for Alzheimer’s cause changed gene expression patterns, indicating a quicker advancement of the disease in their brains.

Regardless of alcohol usage, these findings illuminate the molecular mechanisms driving memory loss and could have wider ramifications for comprehending and treating Alzheimer’s disease.

According to a recent study, mice exposed to regular high amounts of alcohol showed signs of cognitive loss about two months earlier than they would have otherwise.

The onset of Alzheimer’s disease (AD) is sped up by several months or perhaps a few years when ethanol is added to a genetically predisposed population.

While there hasn’t been much research on how alcohol affects Alzheimer’s disease progression, epidemiological studies have found a link between alcohol use disorders and an increased risk of dementia in general.

The researchers carried up an experiment where mice were repeatedly exposed to alcohol over months, simulating the levels of alcohol exposure reported in people with alcohol use disorders. This was done to study the effect of alcohol on Alzheimer’s disease.

They compared the actions of mice with three particular gene mutations linked to an increased risk of Alzheimer’s disease to animals without these abnormalities.

Is there a link between alcohol use and dementia?

The director of the Mary S. Easton Centre for Research and Care at UCLA and a professor of neurology at UCLA, Dr. Keith Vossel, who was not involved in the study, told us that the current research appears to support earlier results about dementia and alcohol use.

According to Dr. Vossel, drinking too much alcohol—more than 21 units per week—has been linked to an increased risk of dementia.

The new study is “fascinating, and the more research that can be done on neurodegenerative diseases like Alzheimer’s disease, the more answers that can then be obtained,” said Dr. Nima Majlesi, an emergency medicine physician and director of Medical Toxicology at Staten Island University Hospital who was also not involved in the study.

There has never been any question in the medical community that excessive alcohol consumption and frequent intoxication [are] unhealthy. On occasion, people have questioned if consuming a small amount of alcohol each day can be healthy. Excessive alcohol consumption and recurring drunkenness [have] many negative impacts on human health, even in patients who are not at risk for [Alzheimer’s disease],” Dr. Nima Majlesi is a doctor.

Dr. Majlesi nevertheless expressed concern, saying that “in this study, they exposed mice to ethanol vapors, which is not the typical route for human consumption.”

We are aware that drinking by inhalation can result in higher brain alcohol concentrations than drinking by mouth. When exposure to ethanol avoids the [gastrointestinal] tract, the metabolism is altered. This may result in some variables that make it a little more challenging to understand the study, according to Dr. Majlesi.

Drinking alcohol and genetic risk may accelerate Alzheimer’simer’s

The current study’s findings showed that mice exposed to alcohol showed a steady loss in their capacity to learn and retain spatial patterns. In addition, these cognitive deficits were present in the alcohol-exposed mice at a younger age than in the control group.

Before the traditional period when such deficits would show, the researchers saw cognitive impairments in the mice treated with alcohol about two months earlier.

The researchers examined gene expression in the brains of mice that had been exposed to alcohol and mice that had not in great detail in order to comprehend the underlying mechanisms of alcohol use disorder.

They compared the gene expression profiles of over 100,000 different cells under examination. The findings showed that prefrontal brain gene expression was significantly altered after alcohol intake.

In particular, the mice that had been exposed to alcohol showed elevated expression of genes linked to inflammation, neurodegeneration, and neural excitability.

Supporting cells including astrocytes, microglia, and endothelial cells also showed altered gene expression patterns in response to alcohol exposure, indicating that these modifications weren’t just restricted to neurons.

Before, it was thought that only neurons could account for the symptoms of Alzheimer’s. These other cell types have just lately been found to have a part in the progression of the disease.

Alcohol changes gene expression may lead to memory loss

The gene transcription profiles of alcohol-exposed mice and control mice at various ages and stages of Alzheimer’s disease but with the same genetic background were compared by the researchers.

They found that the alcohol-exposed mice’s gene transcription profiles resembled older mice who were exhibiting more severe cognitive deterioration rather than mice their own age.

The researchers found that alcohol exposure changed the gene expression patterns in a way that was typically associated with advanced stages of the disease when they compared the alcohol-exposed mice to the same type of mice at various stages of Alzheimer’s disease progression, including mice without any impairments and severely compromised mice.

The significant findings were emphasized for us by Dr. David Hunter, an assistant professor of neurology at McGovern Medical School at UTHealth Houston who was not involved in the study. He explained:

“In this investigation, mice were given alcohol. Some of the mice had the Alzheimer’s disease-causing human genes. Normal control mice were the others. In comparison to sober mice, mutant mice exposed to alcohol experienced cognitive damage early. Neither alcohol nor the control mice were affected.

Dr. Hunter continued, “The researchers also examined gene expression in the mice and discovered that the mutant group that had alcohol had some differences from the sober mutants.”

Mice do not naturally develop Alzheimer’s disease, therefore creating animal models of the condition is intrinsically difficult. We must introduce numerous lethal mutations to them,” said Dr. Hunter.

Does drinking affect dementia in other ways?

According to Dr. Majlesi, “Common sense tells us if we eat clean healthy foods daily, maintain a healthy weight, exercise daily, sleep well, and have little stress, we decrease our risk for several diseases.”

In his statement, Dr. Hunter noted that “neurologists are well aware that chronic and excessive alcohol consumption is bad for the brain.”

Alcohol is a statistical risk factor for all dementia causes, as this article’s opening states. Even in sporadic patients, it appears likely that it speeds up the development of Alzheimer’s pathology. This article clarifies how that link’s mechanism works. The primary takeaway for the general population is that cutting back on alcohol consumption is great advice for keeping in shape.

There is a condition known as alcoholic dementia, a neurodegenerative illness unrelated to Alzheimer’s. It manifests as alterations in visuospatial processing and executive function. The signs are similar to those of Alzheimer’s, according to Dr. Hunter.

Dr. Vossel concurred and said, “There is also a rare form of dementia called Marchiafava-Bignami Disease associated with excessive alcohol intake and malnutrition.”

“More study on this subject is necessary. According to Dr. Vossel, this study “provides evidence that excessive alcohol consumption can affect genetic changes in the brain related to Alzheimer’s disease.”


For Alzheimer’s disease medications that have been suggested by doctors worldwide are available here

Leave a Reply

Your email address will not be published.