SALT LAKE CITY, Utah (ABC4) – Scientists uncovered a possible link to restoring sociability in those who have autism.

Autism is a brain developmental disability that causes problems with social interaction and communication and may have restrictive or repetitive behaviors or interests. It does not have any one particular cause. However, University of Utah researchers may have identified a key trait to help those with autism. 

“[This study] really surprised me because I would’ve thought disrupting brain development when you’re an embryo would be irreversible,” said Randall T. Peterson, Ph.D., the corresponding author of the study and dean of the University of Utah College of Pharmacy. “If you don’t develop sociality as an embryo, you’ve missed the window. But this study suggests that even in those individuals later in life, you can still come in and inhibit this pathway and restore sociality.”

Researchers studied the TOP2A gene, which controls a network of genes associated with causing autism, and it could serve as a link between genetic and environmental factors that could onset the disorder. 

Scientists suspected that many social traits were determined by birth, but this might not necessarily be the case. Research suggests that social behavior, characteristics and traits may not be influenced by genetic makeup, but by how and where we live. 

To test this, scientists tested zebrafish embryos with 1,100 known drugs, one drug per 20 embryos, for 72 hours beginning three days after conception on whether these drugs would influence social behaviors. 

The researchers discovered that four of the 1,120 tested drugs significantly reduced sociability in the zebrafish. All four of these drugs were medications that belong to the same class of antibiotics called fluoroquinolones. These drugs treat upper and lower respiratory tract infections in individuals. 

When the scientists gave related drugs to pregnant mice, those offspring also were less likely to interact with other mice, and these mice also engaged in more repetitive acts, like repeatedly poking their heads in the same hole, than other rodents. 

These drugs suppressed the TOP2A gene, the very gene that acts on a cluster of genes known to cause autism in humans. The gene cluster also binds a group of proteins called PRC2.

Researchers hypothesized that TOP2A and PRC2 work together to create many of the autism-associated genes. 

When the experimental drug UNC1999 was administered to the anti-social zebrafish, those fish were more likely to swim closer and interact with their peers.

Researchers found only four compounds to inhibit the TOP2A gene, but evidence suggests that hundreds of other drugs and naturally occurring compounds in the environment could also be determining factors. 

“It’s possible that these four compounds are just the tip of the iceberg in terms of substances that could be problematic for embryonic exposure,” Peterson said.

Peterson did note that these studies were conducted on animals and not humans. More research needs to be done to confirm this theory. 

“We have no evidence that fluoroquinolones or any other antibiotic causes autism in humans,” Peterson said. “So, there is no reason to stop using antibiotics. What this paper does identify is a new molecular pathway that appears to control social development and is worthy of further exploration.”

The study, conducted by University of Utah Health researchers and colleagues nationwide, appears in the Nov. 23 issue of Science Advances.