Researchers Identify Role of Key Brain Signaling Protein in Alcohol Use Disorder

The Role of Key Brain Signaling Protein Discovered by Researchers Provides New Insights Into (AUD) Alcohol Use Disorder

The causes of alcoholism—or, alcohol use disorder (AUD), as it is now more commonly known—are complicated. Numerous risk factors have been identified as potential causes, but none of them work on a one-size-fits-all category applicable to each distinctive case of AUD. Genetics might play a prominent role in some cases of AUD, while trauma might have a primary role in other cases. A person’s distinct brain chemistry might influence the development of AUD, as can how one is affected by their upbringing and/or early experiences with drinking. More typically, multiple factors are involved in increasing the probability of developing the disorder. The only definitive risk factor involved with all cases of AUD is the consumption of alcohol itself.

Scientists have long studied how the consumption of alcohol affects brain chemistry in efforts to determine the causes of alcoholism at the microbiological level and to seek out potential cures.

Researchers at the Scripps Research Institute recently added to this knowledge pool by discovering how alcohol impacts a region of the brain with key roles in emotional response, behavior, and motivation. The researchers found that alcohol-induced changes to inflammatory mechanisms and cellular activity in the amygdala compromise immune response in the brain, which in turn drives anxiety and alcohol consumption that can lead to the development of AUD.

In their report—“IL-10 normalizes aberrant amygdala GABA transmission and reverses anxiety-like behavior and dependence-induced escalation of alcohol intake”—the Scripps researchers explain how chronic alcohol abuse significantly reduces levels of a key protein with anti-inflammatory properties within the amygdala. The immune protein, Interleukin 10 (IL-10) ensures that the immune system does not over-respond to disease threats and helps limit inflammation in the brain from injury or disease, such as stroke or Alzheimer’s.

Researchers had already deduced from previous studies that IL-10 appeared to influence behaviors related to chronic alcohol abuse and that chronic alcohol use boosts overall IL-10 levels in the brain, but significantly decreases levels within the amygdala itself.

This most recent study was used to specifically test whether low levels of IL-10 in the amygdala played a role in alcohol dependence. To test their theories the researchers boosted IL-10 levels in the amygdala regions of mice that had been conditioned with prolonged alcohol use. Subject mice displayed an addiction to alcohol, as well as low levels of IL-10 in the amygdala. When their amygdala IL-10 levels were artificially boosted, the mice displayed a significant reduction in anxiety-like behaviors and in their compulsion to consume excessive amounts of alcohol.

“We’ve shown that inflammatory immune responses in the brain are very much at play in the development and maintenance of alcohol use disorder,” said lead researcher Dr. Marisa Roberto. “But perhaps more importantly, we provided a new framework for therapeutic intervention, pointing to anti-inflammatory mechanisms.”

The study complements other recent findings by Roberto’s team at Scripps. Future studies will build on all of their findings to identify IL-10 signal pathways in the amygdala and determine whether they play a role in other addiction-related brain circuits.

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Sources:

Scripps Research Institute. “Chronic Alcohol Use Reshapes the Brain’s Immune Landscape, Driving Anxiety and Addiction.” Nov. 16, 2020. Neuroscience News. Retrieved at: neurosciencenews.com

Roberto, Marisa, Ph.D.; Patel, Reesha R., Ph.D.; et. al. —“IL-10 normalizes aberrant amygdala GABA transmission and reverses anxiety-like behavior and dependence-induced escalation of alcohol intake.” Nov. 13, 2020. Progress in Neurobiology. Retrieved at: sciencedirect.com