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HomeLatest NewsHeavy Alcohol Consumption Linked To Increased Brain Inflammation

Heavy Alcohol Consumption Linked To Increased Brain Inflammation

Key Highlights

  • Scientists at Scripps Research have found elevated levels of the immune signaling molecule IL-1β in the brains of mice with alcohol consumption, which could explain some of the risky decision-making and impulsivity in people with AUD.
  • It could also suggest potential treatment with existing anti-inflammatory drugs targeting the IL-1β pathway.

Researchers at Scripps Research have identified a potential new target for developing drugs to treat alcohol use disorder (AUD).

The study, published in Brain, Behavior, and Immunity, suggests that the immune system plays a role in the cycle of AUD and that existing anti-inflammatory drugs targeting the interleukin 1β (IL-1β) pathway could be repurposed to treat the condition.

AUD is characterized by uncontrolled and compulsive drinking and can disrupt communication pathways in the brain, escalating drinking behavior and further exacerbating the condition.

Study Findings

The study found that the levels of IL-1β were elevated in the brains of mice with alcohol consumption. In mice with alcohol dependence, the IL-1β pathway operates differently, causing inflammation in important brain regions linked to decision-making.

According to Marisa Roberto, senior author of the study, these brain inflammatory changes could explain some risky decision-making and impulsivity in people with AUD.

The researchers compared alcohol-dependent mice with animals drinking moderate or no alcohol at all and found that the alcohol-dependent group had about twice as much IL-1β in the medial prefrontal cortex (mPFC), a part of the brain that plays a role in regulating emotions and behaviors.

The team then showed that IL-1β signaling in the alcohol-dependent group was increased and fundamentally different. In alcohol-dependent mice, IL-1β activated pro-inflammatory signaling and boosted levels of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA), likely contributing to some changes in brain activity associated with AUD. These changes in IL-1β signaling persisted even during alcohol withdrawal.

Drugs that can inhibit the function of IL-1β are currently authorized by the US FDA for treating inflammatory ailments such as rheumatoid arthritis. The researchers plan to follow up on this study with more work on how targeting specific components of the IL-1β pathway might be useful in treating AUD.

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