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A new Columbia University brain study on mice has promising results for the estimated 1 in 68 children in the U.S. who are on the autism spectrum.
The research team found that the cortexes of autistic children’s brains were at least 50 percent more densely packed with synapses than normal brains. Synapses are the links between neurons that allow them to communicate — too many of them means the neuron is receiving excess data, much of which is irrelevant.
Neuroscientists were able to reverse autistic behaviors, such as difficulty socializing, by giving the mice an immunosuppressant commonly used to prevent organ rejection after a transplant. The drug was able to restart the natural process of synaptic pruning.
Though a definitive link between brain overconnectivity and autism has not been established, many of the genes known to be present in autistic individuals play a role in synapse pruning.
It is not clear if too many synapses are the main reason for autism, but many genes linked to autism play a role in synapse pruning. And the discovery that synapse pruning reversed autistic behavior in the lab mice suggests overconnectivity may be key.
While the results are promising, the drug used in the study, rapamycin (sold by Pfizer as Rapamune), can cause serious side effects because of its aggressive suppression of the immune system.
One remaining puzzle is how the mice’s brains, or the drug, know which synapses to keep and which to prune. Dr. David Sulzer, who led the study, said “the mice started behaving normally” after receiving the synapse-pruning drug, “which suggests the right ones are being pruned.”
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