Science

Genetic technique improves visual learning in mice with autism

Genetic technique improves visual learning in mice with autism
An experimental technique boosted activity in areas of the visual cortex, helping autistic mice learn a visual task as fast as their healthy counterparts
An experimental technique boosted activity in areas of the visual cortex, helping autistic mice learn a visual task as fast as their healthy counterparts
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An experimental technique boosted activity in areas of the visual cortex, helping autistic mice learn a visual task as fast as their healthy counterparts
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An experimental technique boosted activity in areas of the visual cortex, helping autistic mice learn a visual task as fast as their healthy counterparts

A fascinating new study from scientists at UCLA has proposed a novel strategy to help autistic individuals improve their ability to process visual information. The experimental technique, demonstrated in mice, found that certain dysfunctional cells in the visual cortex can be genetically "tuned" to better respond, allowing improved visual and sensory learning abilities.

"The focus in autism has been trying to tackle social impairment," explains Anubhuti Goel, first author on the new study. "But if there is a deficit in learning due to being unable to process certain kinds of sensory input, it affects your development. We're trying to identify early brain processes that will impact behaviors in children when they are older."

The research focused on mice engineered to have fragile X syndrome (FXS), a single-gene disorder commonly related to inherited autism in humans. While other research into FXS has examined behavioral symptoms associated with the condition, such as repetitive or obsessive patterns, this study looked at how to improve learning dysfunctions. Using the template of a certain visual discrimination task, the researchers found that healthy mice could learn a new water-gathering strategy after three days while the FXS animals, on average, needed five to nine days to grasp the new skill.

It was revealed that the FXS mice displayed several cellular deficiencies in their visual cortex. They had less pyramidal cells, excitatory neurons fundamental to perceiving orientation in visual information, and they showed less activity in parvalbumin neurons, a kind of inhibitory neuron that helps pyramidal cells respond to sensory stimuli.

So the researchers developed a unique genetic technique designed to activate the parvalbumin neurons, subsequently improving the activity of the pyramidal cells. A virus was engineered to carry genes to the animal's parvalbumin cells and generate new receptors programmed to be triggered into activity by the administration of a designer drug. The technique was dubbed DREADD: Designer Receptors Exclusively Activated by Designer Drugs.

The results were incredibly effective. When administered the designer drug, the FXS mice were amazingly able to learn the visual discrimination task as fast as healthy mice. This suggests that FXS-related learning difficulties could be effectively modulated by manipulating visual sensory processing.

"These experiments shed light on the brain circuit problems behind those difficulties in autism, and hint at directions we can pursue for treatment in the future," says Goel.

At this stage much of the research is academic, after all we are not exactly near a point in history where we can safely deliver these kinds of treatments to human children. But, the work does offer intriguing insights into how autistic brains may be processing sensory information differently to an average brain, and how that could hypothetically be improved.

The next step for the UCLA researchers is to examine how sensory distractions are processed by FXS brains. It's common for autistic children and adults to have over-reactions to external sensory stimulation, such as loud sounds, so understanding how brains can better tune out distracting stimuli may help improve learning skills.

The research was published in the journal Nature Neuroscience.

Source: UCLA

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