Alcohol use disorder (AUD) is a condition where people have difficulty controlling their alcohol intake, leading to uncontrolled and compulsive drinking.
AUD can cause changes in the brain, which can lead to further changes in behavior, creating a vicious cycle.
In a recent study, scientists at Scripps Research have found new information about the immune system’s role in this cycle.
They found that a signaling molecule called interleukin 1β (IL-1β) plays a crucial role in the inflammation of the brain of mice with alcohol dependence.
Inflammation can occur in areas of the brain that are critical for decision-making, leading to risky behavior and impulsivity in people with AUD.
The researchers believe that their findings offer potential for treating AUD with existing anti-inflammatory drugs that target the IL-1β pathway.
Drugs that block the activity of IL-1β are already approved by the U.S. Food and Drug Administration to treat rheumatoid arthritis and other inflammatory conditions.
The team showed that mice with alcohol dependence had about twice as much IL-1β in a part of the brain called the medial prefrontal cortex (mPFC) compared to mice drinking moderate or no alcohol at all.
The mPFC is responsible for regulating emotions and behaviors.
Furthermore, IL-1β signaling in the alcohol-dependent group was not only increased but also fundamentally different from the moderate or no alcohol groups.
In mice that had not been exposed to alcohol, as well as in mice that had drunk moderate amounts of alcohol, IL-1β activated an anti-inflammatory signaling pathway.
This lowered levels of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), which regulates neural activity in the brain.
However, in alcohol-dependent mice, IL-1β activated pro-inflammatory signaling and boosted levels of GABA, contributing to changes in brain activity associated with AUD.
Notably, these changes in IL-1β signaling in the alcohol-dependent mice persisted even during alcohol withdrawal.
Previous studies have already shown links between the immune system and AUD, particularly around IL-1β.
People with certain mutations in the gene that codes for the IL-1β molecule are more prone to developing AUD. Additionally, autopsies of people with AUD have found higher levels of IL-1β in the brain.
The researchers plan to follow up on this study by investigating how targeting specific components of the IL-1β pathway could be useful in treating AUD.
It’s important to note that more work is needed to determine whether existing drugs that block the activity of IL-1β could be useful in treating AUD.
The discovery of the role of IL-1β in AUD is exciting news for people with this condition and for scientists studying it.
It opens up new avenues for treatment and brings us closer to understanding the complex mechanisms that underlie AUD.Top of FormBottom of Form
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The study was conducted by F.P. Varodayan et al and published in Brain, Behavior, and Immunity.
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