MIT scientists have successfully reversed autistic-like behavioral patterns in mice. The study focused on a gene called Shank3, which is missing in 1 percent of individuals suffering from autism, and is believed to be vital for the development of a healthy adult brain.
Autism is a term for a group of disorders that arise from a diverse range of genetic causes that work to prevent the brain from developing normally, often making the simplest of social interactions incredibly difficult. According to the US Centers for Disease Control and Prevention (CDC), instances of autism have risen 10-fold over the space of 40 years, with roughly 1 in 68 American children currently thought to be on the autistic spectrum.
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The new MIT research may lead to gene therapy treatment for some patients that could alleviate certain behavioral defects synonymous with autism. Prior to the study, the Shank3 protein was known to be located in the brain's synapses, where it acts as a scaffold for other proteins, organizing them and allowing them to work together to allow a neuron to form a cohesive response to an incoming signal.
Scientists have observed that mutations or deficiencies of Shank3 in the brain can cause synaptic disruptions in mice, leading to some of the irregular behavioral patterns linked to autism. Furthermore, researchers have noted a lower quantity of dendritic spines in mice suffering from a Shank3 deficiency, with the abnormality becoming more pronounced in the striatum.
For the purposes of the recent study, scientists genetically engineered mice with inactive Shank3 genes. As the mice developed, they exhibited a number of autism-like behaviors including an aversion to social situations, compulsive and repetitive behavior, and anxiety.
Between two to four months after birth, the team introduced a breast cancer drug known as tamoxifen into the food of the mice, which had the effect of reactivating the Shank3 in the rodents' synapses.
Soon after, the team noticed alterations in the behavior of the mice, including an absence of repetitive actions and an increase in socializing. Mice that were introduced to the tamoxifen at an earlier stage also appeared to display a reduction in anxiety and improved motor skills.
The results of the study display a surprising level of elasticity on a cellular level, with the brain proving to be capable of rewiring itself and generating new dendritic spines.
The next step for the team will be to discern at what point circuits in the brain relating to anxiety and motor function become too damaged to respond to the newly activated Shank3 proteins.
"Some circuits are more plastic than others," states lead author of a paper on the findings Guoping Feng, a professor of brain and cognitive sciences at MIT. "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."