According to recent research conducted by scientists at Scripps Research and the University of Bologna, it is advised that individuals with a genetic predisposition toward dementia should be cautious about consuming alcohol. The study found that alcohol use disorder (AUD) can accelerate the progression of Alzheimer’s disease in individuals with a genetic susceptibility to the condition.
Researchers discovered that repeated alcohol intoxication in mice genetically predisposed to Alzheimer’s resulted in changes in gene expression associated with disease progression. These mice displayed signs of declining brain health approximately two months earlier when regularly intoxicated.
According to co-lead author Federico Manuel Giorgi, a Computational Genomics professor at the University of Bologna, the inclusion of ethanol in a genetic context related to Alzheimer’s disease accelerates the progression of the condition by a span of several months or even years.
Several studies have suggested a possible connection between alcohol use disorder (AUD) and an increased risk of dementia. To further investigate the impact of alcohol on Alzheimer’s disease, researchers exposed mice to alcohol levels similar to those consumed by individuals with AUD for several months. A control group of mice was also included, along with mice carrying three genes known to elevate the risk of Alzheimer’s.
The results revealed that the alcohol-exposed mice exhibited worsening cognitive abilities, such as difficulty learning and remembering spatial patterns, and showed cognitive decline signs earlier than anticipated, compared to the control group.
Co-lead author Peitro Sanna, an Immunology and Microbiology professor at Scripps Research said that they observed cognitive impairments in the mice treated with alcohol around two months earlier than their typical onset.
The researchers conducted a study to understand the effects of alcohol use disorder on brain cells. Findings revealed that alcohol exposure leads to significant changes in gene expression in the prefrontal cortex. The affected genes were associated with increased neuronal excitability, inflammation and neurodegeneration. These changes were observed not only in neurons but also in supporting cells like microglia, astrocytes, and endothelial cells.