MIT and Harvard University researchers have discovered that autistic behavior is linked to a breakdown in the signaling pathway that is used by a primary inhibitory neurotransmitter that is called GABA.
Robert Preidt, a reporter for HealthDay, writes that the study was published in the journal Current Biology expressed that:
“This is the first time, in humans, that a neurotransmitter in the brain has been linked to autistic behavior. This theory — that the GABA signaling pathway plays a role in autism — has been shown in animal models, but until now we never had evidence for it actually causing autistic differences in humans,” study leader Caroline Robertson said in a university news release.
The research team found the link through the use of brain imaging and a visual test that triggers different reactions in the brains of those with autism and those without the condition. The scientists believe that tests like these could eventually be used to screen young people for autism.
For some time, GABA has been a suspected factor in autism, but until now, there was no substantial proof. Robertson noted that people with autism frequently have seizures, and about 20% to 25% of patients have a combination of autism and epilepsy.
The new finding does improve understanding of the disorder, and the possibility of the development of new treatments is real, but GABA is just one piece of the puzzle, say the researchers. They add that they would continue to screen the autistic brain for additional pathways that may play a role. Despite this discovery, other experts caution that the overall causes of autism are yet to be found.
GABA is one of the multiple neurotransmitters that scientists have suspected of playing a part in the autism spectrum disorder (ASD). GABA lessens some of the neurons’ signals, so the brain focuses on the transmissions that seem more important at the moment. An example: when a person looks at an object, the brain receives two images, one from each eye. GABA allows the brain to bring the two images into one, writes Cameron Scott of Healthline.
Robertson and her team studied this visual processing to understand how GABA worked in participants in the study with ASD and those without the disorder.
In the 20 people with ASD, GABA did not lessen selective neurons. Glutamate, another neurotransmitter on the suspect list for autism researchers, worked in a normal way.
Since GABA is not able to subdue the neurons, it implies that there is a dysfunction in the pathway. An example of this kind of malfunctioning pathway in the brain is depression. SSRIs, or selective serotonin reuptake inhibitors, treat depression because they allow more serotonin to be used by the neurons as they communicate.
Researchers hope that a drug which is able to change the way neurons use GABA could result in quieting the symptoms of autism.
Richard Edden, an associate professor of radiology at the Johns Hopkins University School of Medicine, reacted to the study by saying:
“This is a really great piece of work. The role of inhibitory dysfunction in autism is strongly debated, with different camps arguing for elevated and reduced inhibition. This kind of study, which seeks to relate measures of inhibition directly to quantitative measures of function, is what we really to need to tease things out.”
This study may also help by offering researchers the opportunity to develop more and better diagnostic tools for ASD and by providing a tool for earlier intervention. Currently, autism is diagnosed by evaluating the social interactions of children, writes Anne Trafton for the MIT News Office.
