Specialists in addiction care know that alcoholics seeking sobriety may struggle with depression. Drinking is then often resumed as a form of self-medication for that depression.
A study by researchers at the University of Illinois/Chicago’s (UIC) Center for Alcohol Research in Epigenetics looked at the problem by identifying areas in the brain that may be implicated in this depressive state.
The study, published in the journal Translational Psychiatry, is titled “Transcriptomics identifies STAT3 as a key regulator of hippocampal gene expression and anhedonia during withdrawal from chronic alcohol exposure.”
The UIC researchers chose an area of the brain called the hippocampus to look for answers.
Starting first with post-mortem hippocampus samples from rats and then humans, the team discovered that alcohol withdrawal seems to change cells’ genetic expression in this region of the brain.
This change in gene expression affects the manufacture of a protein called STAT3. During alcohol withdrawal, these genes seem to call for an increase in the production of STAT3.
Intrigued, the research team treated rats with a drug that blocked STAT3 production and found the ability of the rats to feel pleasure improved.
Researchers believe this discovery in rats may lead to drug therapies that block STAT3 production in humans during alcohol withdrawal, thus increasing long-term sobriety and recovery chances.
According to one of the lead researchers, Amy Lasek, UIC associate professor of psychiatry and anatomy and cell biology, “We know that chronic alcohol use can induce an immune response in the brain. By inhibiting STAT3, we think that we are dampening that hyperactive immune response (often associated with depressive states) by blocking the ability of STAT3 to increase the expression of these immune-response genes during withdrawal.”
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