Immune molecule may contribute to excessive drinking in alcohol use disorder

by The Scripps Research Institute

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The drugs that keep rheumatoid arthritis in check may one day help people stop drinking. A new Scripps Research study shows that an anti-inflammatory molecule, already approved by the U.S. Food and Drug Administration to treat autoimmune diseases, reduces excessive alcohol consumption in alcohol-dependent female mice.

The new findings, published in the Journal of Neuroinflammation, add to a growing body of evidence that brain inflammation is involved in alcohol use disorder.

"This disorder is, in part, driven by damage to our neuroimmune system," said senior author Marisa Roberto, professor of translational medicine and the Paul and Cleo Schimmel Endowed Chair at Scripps Research. "Targeting this system might be an exciting clinical avenue to follow up with in the coming years."

IL-6 draws a closer look

The new research revolves around a molecule called interleukin-6, or IL-6, which the body produces in response to stress, infection and injury. Best known for its role in driving inflammation in diseases like rheumatoid arthritis, IL-6 is produced not just by immune cells throughout the body but also by cells in the brain, where it can directly influence brain circuit functions.

Previous research had already suggested that people who drink heavily tend to have elevated levels of IL-6 in their blood, and that a genetic variant in the IL-6 gene is associated with an increased risk of alcohol use disorder. Due to these associations, Roberto's team wondered whether blocking IL-6 could reduce drinking behavior.

How IL-6 affects brain signaling

To test that idea, the researchers turned to a mouse model of alcohol use disorder in which animals have escalating and compulsive drinking behavior. They confirmed that chronic alcohol exposure increased levels of IL-6 signaling in the brain's central amygdala, a region tied to addiction behaviors. They then showed that in alcohol-dependent mice, IL-6 suppresses the central amygdala's GABA system, which usually prevents neurons from becoming overactivated.

"GABA is an important brake signal that the brain uses to dampen the activity of neurons," explained co-first author Chloe Erikson, a postdoctoral fellow in the Roberto lab. "When this braking system gets weakened, overexcitation can result. That loss of inhibitory control plays a large role in alcohol use disorder-associated behaviors like alcohol consumption, craving and withdrawal."

A response seen in females

Next, the group gave alcohol-dependent mice an antibody targeting the IL-6 receptor—the same class of drug used for rheumatoid arthritis. The antibody works by binding to the IL-6 receptor, preventing IL-6 from acting on cells throughout the body, including the brain. After receiving the treatment, alcohol-dependent female mice drank significantly less alcohol. Dependent males, in addition to nondependent animals of either sex, showed no significant change, suggesting the drug wasn't broadly suppressing drinking but acting on a specific, dysregulated molecular pathway that drove drinking behavior in the females.

"In the human literature, we know that women are more prone to autoimmune diseases, so while the positive results in our female mice were surprising, they aligned with the clinical data," said co-first author Celsey St. Onge, also a Scripps Research postdoctoral fellow.

The results point to meaningful biological differences in how male and female brains respond to alcohol use disorder. However, the researchers note that more work is needed to untangle the sex difference; female mice in the study also drank more alcohol than males, which could explain some of the difference in treatment response.

Human brain tissue shows the same signal

In addition to the mouse studies, the team analyzed postmortem brain tissue from 30 humans diagnosed with alcohol use disorder and 30 people without it. They identified 377 differentially expressed genes between the two groups. Among the strongest signals was IL-6, which was significantly elevated in those with alcohol use disorder, along with several other inflammation-related genes.

Beyond their specific finding, the researchers say the work speaks broadly to how scientists view alcohol use disorder. Roberto's lab has previously linked another immune protein in the brain to alcohol withdrawal symptoms and has tested a different anti-inflammatory drug for its potential to treat alcohol use disorder.

"There has been a substantial shift in the field in the past few years to classify alcohol use disorder as a whole-body disease," Roberto said. "With this neuroimmune angle, we add to the growing literature that drinking too much can take a serious toll on your health. It's our hope that classifying it as such can continue to destigmatize this complex disorder."

Publication details

Celsey M. St. Onge et al, Translational evidence for increased central amygdala IL-6 activity in alcohol dependence, Journal of Neuroinflammation (2026). DOI: 10.1186/s12974-026-03868-2

Journal information: Journal of Neuroinflammation

Key medical concepts

Alcohol use disorderCentral Amygdaloid Nucleus

Clinical categories

PsychiatryPsychology & Mental health Provided by The Scripps Research Institute Who's behind this story?

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