A new study published on autism gives new hope to patients. The disorder could be due to an overabundance of connections between neurons. A new treatment could emerge.
New step on the road to understanding and healing autism? American researchers have indeed shown that an overabundance of synapses, the nerve connections between neurons in the brain, could be at the origin of the disorder.
In recent months, research on autism has continued to advance, and the results of this work reinforce this trend, as they could potentially pave the way for new treatments. This is good news, whereas in France, one in 100 births is affected by this disorder, and about 650,000 people are affected.
In May, a team of Canadian researchers had developed a more reliable autism screening formula, studying more than 1,700 genetic mutations. Their discoveries could help to better orientate treatments, and cure autism earlier. An objective they share with the authors of the latest study.
Unnecessary synapses
This latest work was carried out by researchers at Columbia University, New York, and published in the scientific journal Neuron. They examined the brain, and more specifically the cerebral cortex, of 48 young people who died when they were between 2 and 20 years old. Of these, 26 had autism.
In babies and toddlers, the brain produces large amounts of synapses. It is through these synapses that neurons transmit and receive signals. Subsequently, the brain removes some of these connections so that its different parts can develop quietly, without excess signals, and without confusion.
Thus, in a 19-year-old non-autistic child, the brain is made up of 41% fewer synapses than in a two-year-old. However, according to these researchers, for a 19-year-old with autism, this is only 16% fewer connections. This overabundance of synapses is therefore explained by a dysfunction of the mechanism for eliminating unnecessary synapses.
In mice
Next step: test the practical applications of this discovery on the mouse. Rodents, genetically modified to simulate autism, have been treated with an anti-proliferator, rapamycin, which blocks the action of the mTOR protein, responsible for cell proliferation and growth. The researchers thus succeeded in restoring the synapse pruning mechanism. As a result, some symptoms of autism, such as avoiding contact with others, disappeared in these mice. This is therefore an argument in favor of the use of rapamycin, which could be adapted in certain treatments for autism, in order to reduce some of the symptoms.
Much hope had also been raised in June by suramin, the drug that treats sleeping sickness in Africa, this one having been tested successfully on the same type of mouse, genetically modified. It had made it possible to eliminate all the symptoms of autism in guinea pigs, but with a limited effectiveness in time.
In both cases, clinical trials on human subjects are expected to begin shortly.
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