A new study by Massachusetts Institute of Technology researchers has successfully reversed some of the behavioral symptoms of autism in mice, allowing their brains to properly rewire themselves.
Autism is a disorder that has many diverse genetic causes, many of which have yet to be uncovered by scientists. However, approximately 1 percent of people with autism are missing a gene called Shank3, which is crucial for the proper development of the brain. Individuals missing this gene develop symptoms connected to autism such as repetitive behavior and avoidance of social interactions.
In the current study, the team turned this gene back on in mice later on in their lifespan, showing that many of the effects of autism have the potential to be reversed.
"This suggests that even in the adult brain we have profound plasticity to some degree," Guoping Feng, senior author of the study, said in a press release. "There is more and more evidence showing that some of the defects are indeed reversible, giving hope that we can develop treatment for autistic patients in the future."
Shank3 is located in neuron synapses and helps organize the hundreds of proteins that are necessary to ensure the proper response of neurons to incoming electrical signals. Brains missing this gene experience synaptic disruptions, which leads to compulsive behavior, anxiety and the avoidance of social interaction.
For the new study, Feng and his team created genetically engineered mice that had their Shank3 gene turned off during development, but also had the ability to have it turned back on by the addition of taxomifen to their diet.
The results showed that turning Shank3 on two to four and a half months after birth resulted in the elimination of repetitive behavior and their tendency to avoid social interaction. Furthermore, this increased the density of dendritic spines in the striatum of the mice, which shows structural plasticity in the adult brain. However, anxiety and motor coordination symptoms did not disappear.
Feng hypothesized that anxiety and motor coordination are behaviors that rely on circuits that were formed early on during development and are likely irreversible. To test this hypothesis, he activated Shank3 earlier in some mice, just 20 days after birth, and found that anxiety and motor coordination improved.
"Some circuits are more plastic than others," Feng said. "Once we understand which circuits control each behavior and understand what exactly changed at the structural level, we can study what leads to these permanent defects, and how we can prevent them from happening."
The findings were published in the Feb. 17 issue of Nature.
