A new study by neuroscientists at Harvard and MIT has identified a link between the activity of the neurotransmitter GABA and symptoms of autism, Huffington Post reports.
"This is the first connection in humans between a neurotransmitter in the brain and an autistic behavioral symptom," Caroline Robertson, a postdoc at MIT's McGovern Institute for Brain Research and the study's lead author, said in a statement.
The findings were published online Dec. 17 in the journal Current Biology.
The new finding will pave the way for new methods of treating and diagnosing autism.
"GABA is responsible for signaling that neurons should turn off, or stop firing," Robertson told HuffPost. "It tends to come into play ... when information is being transmitted and it needs to be shut down or filtered out."
Scientists feel that a lack of GABA could be the cause of the hypersensitivity to sensory input seen in individuals with autism.
"It's necessary to filter out signals in the external world that aren't relevant to the task at hand," Robertson said. "GABA helps us in this kind of inhibition."
Hypersensitivity to one's external environment makes it difficult for Autistic individuals to filter distracting sounds and sensations.
Previous studies had linked reduced GABA activity with autism-like behaviors in animals. However, no such correlation had been established in people.
For the study, the researchers asked a group of participants to complete a visual task that required brain inhibition. Half of the participants were autistic, while half were not.
The researchers noted that non-autistic participants, who had higher GABA levels, were better able to suppress the non-dominant image. However, there was no relationship between performance on the task and GABA levels in the participants who were autistic.
"It's not as simple as GABA is missing in the autistic brain," Robertson explained.
"It's not in lower concentration, it's just not relating to visual perception."
However, the researchers aren't yet sure of the cause for this dysfunction.
"A lot more work needs to be done," she said.
The study could open up the possibility of new drugs that target GABA pathways and could also lead to examination of GABA activity in early screenings for autism.
"It'll be a longer story than just, Aha! We'll make some GABA-enhancing drugs and cure autism," Robertson said. "But it does point to a pathway that seems to be dysfunctional in the autistic brain."
