Autism: brains are wired too well

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MunichAutistic people have more interfaces in the brain than healthy people. Apparently, their brain maturation takes place differently in their infancy than in their normal peers. American researchers have derived a new therapeutic approach from this - and have already achieved initial successes.

Many connections between the nerve cells in the thinking organ, the so-called synapses, are the prerequisite for a functioning brain. In the first few months of an infant's life, the brain therefore forms a particularly large number of such synapses. They connect the nerve cells and different brain regions almost "randomly". But the older the child gets and the more it learns, the more unnecessary connections are recognized and broken down. Normally - because it is precisely this developmental step that seems to be disturbed in patients with autism, found Dr. David Sulzer and his colleagues at Columbia University Medical Center.

Cell scrap everywhere

To do this, the researchers examined 26 brains of deceased children with autism. 13 of them had lived to be between two and nine years old, and another 13 had died between the ages of 13 and 20. They compared this to 22 brains from children without autism.

They discovered that in the control group the number of synapses had decreased sharply in half of the children, in contrast to only about 16 percent of the cases in the autistic children. In addition, there were many fragments of old cell waste in the autistic brains. An indication that the so-called autophagy does not work properly in autistic people. This "controlled self-digestion" ensures that dead cells or cell components are disposed of or reused.

Disturbed self-digestion

Using the mouse model, the researchers were able to show how this accumulation of cell waste occurs: Just like humans, mice with autism have a particularly large amount of a protein called mTOR in their brain. It slows down the cells' self-digestion and in autistic people ensures that superfluous synapses are not broken down as actually intended. “People always think that it is very important to form new connections in the brain through learning,” says Sulzer. "But it is just as important that incorrect links are broken down."

Autism as a result of a lack of brain differentiation? Sulzer and his colleagues continued their research and treated their autistic mice with a drug called rapamycin. This blocks the effect of mTOR. The therapy was successful in the rodents - even if the animals were already showing autistic behavior. The treatment improved the mice's autistic symptoms. The subsequent examination of their brains showed that their synapse number had also approached that of healthy mice. This indicates that such a therapy could be effective, even if the first symptoms of the developmental disorder have already appeared, according to the scientists.

First common denominator

Many genes are already known that contribute to the development of autism. “What they all have in common is that those who wear them have overactive mTOR and the limited ability to autophagy in the brain,” explains Sulzer. For the first time, a connection would have been found that also offered possibilities for a therapeutic approach. This can also be used to diagnose the disease more easily.

Developmental disorder with consequences

Autism is one of the most profound developmental disorders. Three areas of life are particularly impaired in autistic people: social skills, opportunities for communication and behavior. For example, autistic people find it difficult to build relationships with other people or their ability to speak is impaired. The severity of the autism symptoms varies greatly from person to person. Some children only develop mild autism, others are severely mentally disabled. So far there is no way to treat the cause of autism. (lh)

Source: Guomei Tang et al. Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits. Neuron, 2014; DOI: 10.1016 / j.neuron.2014.07.040

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