Rebalancing an autistic brain

A well-known drug for treating anxiety might serve a new purpose as a therapeutic approach for autism according to the study published in Neuron on March 19th by researchers at the University of Washington.

Currently used for anxiety and patients with epileptic seizures, drugs called benzodiazepines modulate chemicals in the brain.  The chemicals they affect are also ones that potentially cause autism spectrum disorders. Normally, there is an even distribution of excitatory (similar to a gas pedal, stimulating) and inhibitory (similar to applying a brake) cells in the brain, but it has been shown in previous studies this is not the case in autism – that there are more excitatory cells than inhibitory, but William Catterall’s new study shows that the drug can help restore the balance.

Catterall and his research team looked at a mouse model that is commonly used to study autism.  The mice exhibit many of the same symptoms: repetitive behavior, poor social interactions, and even learning difficulties.  Rather than approaching the situation by trying to decrease excitatory cells, Catterall decided to try to increase inhibitory cells. Using low doses of benzodiazepine, Catterall found that the balance was closer to being restored, and autistic behaviors of the mice were diminished.

In autism spectrum disorders there is an imbalance of excitatory and inhibitory cells in the brain. Low doses of anxiety drugs can recreate this balance, decreasing common autistic behaviors, such as poor social skills.

While many research groups are looking for a preventative mechanism for autism, Catterall has provided a great potential therapeutic treatment for those who have the spectrum disorder.  As the results proved very promising in mice, human clinical trials are now needed as a next step.  Astra-Zeneca and the National Institutes of Health are currently initiating a phase II clinical trial.

To read the article:

Han, Sung, et al. “Enhancement of Inhibitory Neurotransmission by GABAA Receptors having α2,3-Subunits Ameliorates Behavioral Deficits in a Mouse Model of Autism.” Neuron 81.6 (2014): 1282-9. Print.

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