New research out of the University of Illinois Chicago (UIC) shows that gene editing may help to cure anxiety and alcohol use disorder in people that had a binge drinking problem as adolescents.
Findings from the study show a more promising approach for combating these disorders that are of great concern globally. These conditions affect millions of adults in America.
Researchers found that gene editing can reverse epigenetic reprogramming that contributes to anxiety and alcohol abuse.
“Early binge drinking can have long-lasting and significant effects on the brain, and the results of this study offer evidence that gene editing is a potential antidote to these effects, offering a kind of factory reset for the brain if you will,” said Dr. Subhash Pandey, senior study author, and the Joseph A. Flaherty Endowed Professor of Psychiatry.
The UIC researchers have been probing what health effects binge drinking in early life can have in later life. They published findings from this new study in Science Advances.
Restoring brain chemistry
Adolescent binge drinking causes some unwanted changes in brain chemistry, the UIC team observed in earlier research. These alterations occur more specifically at the Arc gene’s enhancer region.
Problem drinking in adolescence leads to a reduction of Arc expression in the amygdala of humans and rodents. The amygdala is regarded as the center of emotion and plays a role in memory formation.
The Arc gene’s epigenetic reprogramming that occurs from binge drinking in adolescent years makes a person more likely to have anxiety and alcohol abuse issues in adulthood. It continues all through the life of an affected person.
This new research is interesting in that it shows that gene editing could offer a way out of this epigenetic reprogramming.
Fighting anxiety and alcohol abuse
Researchers made use of a gene-editing method known as CRISPR-dCas9 in this study. They used it to control the histone acetylation and methylation processes of the Arc gene in rat models. These processes manage how accessible genes are for activation.
The team started by examining adult rats that were exposed to alcohol from time to time during adolescence, equivalent to the human age between 10 and 18. It used dCas9 to encourage acetylation, which loosens chromatin and enables the binding of transcription factors to the DNA.
Researchers observed Arc gene expression returning to normal when acetylation improved. There were reductions in indicators of anxiety and alcohol intake.
Pandey and his team examined adult rats that were not exposed to alcohol early in another model. Arc gene expression reduced when dCas9 was used to increase methylation, thereby tightening chromatin and keeping transcription factors from binding to DNA. Anxiety and alcohol use were observed to worsen as a result.
Researchers noted that these findings show that “epigenomic editing in the amygdala can ameliorate adult psychopathology after adolescent alcohol exposure.”
Pandey pointed out that the study helps to shed more light on what is taking place in developing brains exposed to strong alcohol concentrations. It also raises hope of more helpful treatments becoming available someday for anxiety and alcohol use disorder, which are difficult to deal with.
“That this effect was seen bidirectionally validates the significance of the Arc enhancer gene in the amygdala in epigenetic reprogramming from adolescent binge drinking,” he added.