In 2015, 47 million people suffered from Alzheimer’s and other dementias (around 5% of the planet’s population), a figure that could reach 75 million in 2030 and 132 million in 2050, which means that the number of people affected by these pathologies Brain injuries will double every 20 years, according to a report from the Ministry of Health, Consumption and Social Welfare, which collects data from the World Health Organization (WHO).
This gives an idea of the tremendous public health problem they generate. The most frequent type of dementia is Alzheimer’s disease, since it accounts for between 60 and 80% of dementia diagnoses, according to the Alzheimer’s Association. Alcohol use disorder is one of the risk factors for developing Alzheimer’s, so research continues to determine its impact.
A new study has now shown that the consumption of even small amounts of alcohol can accelerate brain atrophy, that is, the loss of brain cells, and increase the presence of amyloid plaques, which consists of the accumulation of toxic beta amyloid proteins that characterize Alzheimer’s. “These findings suggest that alcohol may accelerate the pathologic cascade of Alzheimer’s disease in its early stages,” said Shannon Macauley, an associate professor of physiology and pharmacology at Wake Forest University School of Medicine.
Alcohol consumption alters brain function
The researchers conducted their experiments with mouse models of Alzheimer’s disease, offering them the choice of drinking water or alcohol for 10 weeks to mimic the chronic drinking pattern similar to human behavior. They then looked at how voluntary, moderate alcohol intake altered healthy brain function and behavior and whether it modified pathological signs associated with the early stages of Alzheimer’s disease. The results of the work have been published in Neurobiology of Disease.
“Alcohol use may be a modifiable risk factor for Alzheimer’s disease and dementia”
These scientists found that alcohol consumption increased brain atrophy and caused the development of more amyloid plaques, including more smaller plaques that could contribute to the development of more plaques during aging. On the other hand, they were surprised to find that acute alcohol withdrawal increased levels of amyloid beta, a key component of amyloid plaques that form and accumulate in Alzheimer’s patients.
In another analysis, they found that chronic alcohol exposure downregulated cerebral and peripheral metabolism, another way of accelerating the disorders associated with Alzheimer’s. Previously, Macauley had shown that elevated blood sugar levels increase beta amyloid and amyloid plaques, and in the current work, the researchers found that even moderate alcohol consumption caused blood sugar and markers to rise. insulin resistance, which not only increases the risk of Alzheimer’s, but also other diseases such as type 2 diabetes and cardiovascular disease.
They also found that moderate alcohol consumption influenced anxiety and behaviors related to dementia. “These preclinical findings suggest that even moderate alcohol consumption can lead to brain injury,” Macauley said. “Alcohol use may be a modifiable risk factor for Alzheimer’s disease and dementia.”
The research was led by Macauley and Jeffrey Weiner, professor of physiology and pharmacology at Wake Forest University School of Medicine, in collaboration with the Alzheimer’s Disease Research Center and the Alcohol Translational Research Center at the School of Medicine.
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