A recent study at the Scripps Research Institute showed important changes to anti-inflammatory mechanisms in a brain region that drive alcohol addiction.
Researchers found that chronic alcohol drinking compromises brain immune cells, which are important for maintaining healthy neurons.
The resulting damage fuels anxiety and alcohol drinking that may lead to an alcohol use disorder.
By countering this process, the researchers were able to stop excessive alcohol consumption—revealing a potential treatment path for alcohol use disorder.
The study is published in Progress in Neurobiology. One author is Marisa Roberto, Ph.D.
Deep within the brain, a small almond-shaped region called the amygdala plays a vital role in how we exhibit emotion, behavior and motivation.
The region is also strongly implicated in alcohol abuse.
In the study, the team focused on an immune protein called Interleukin 10, or IL-10, which is prevalent in the brain.
IL-10 is known to have potent anti-inflammatory properties, which ensures that the immune system doesn’t respond too powerfully to disease threats.
In the brain, IL-10 helps to limit inflammation from injury or disease, such as stroke or Alzheimer’s. But it also appears to influence key behaviors associated with chronic alcohol use.
In mice with chronic alcohol use, IL-10 was strongly reduced in the amygdala and didn’t signal properly to neurons, contributing to increased alcohol intake.
By boosting IL-10 signaling in the brain, however, the team could reverse the aberrant effects. Notably, they observed a big reduction in anxiety-like behaviors and motivation to drink alcohol.
These findings showed that inflammatory immune responses in the brain are very much at play in the development of alcohol use disorder.
They also provided a new framework for therapeutic intervention, pointing to anti-inflammatory mechanisms.
Alcohol use disorder is widespread, affecting some 15 million people in the United States, and few effective treatments exist.