Children with autism have higher number of synapses than their peers, a new study shows. The extra neuronal networks are due to the decreased pruning.
The human brain undergoes several changes in the first few years of life. Brains of young children have unnecessary connections that get snipped when they reach puberty. Previous research has even shown that the synaptic pruning continues to occur in the brains of adults who are in their 20s.
The current study, conducted by Columbia University Medical Center (CUMC) scientists, shows that brains of autistic individuals don't lose the extra connections. These neuronal pathways might lead to a change in the way the brain functions.
Drug for Autism?
According to the researchers, drugs that are known to prune the neuronal synapses can be used to control some symptoms of autism. The team conducted studies on mice using the drug rapamycin and found that the drug reduced some autism-like symptoms in test mice.
"This is an important finding that could lead to a novel and much-needed therapeutic strategy for autism," said Jeffrey Lieberman, MD, Lawrence C. Kolb Professor and Chair of Psychiatry at CUMC and director of New York State Psychiatric Institute, who was not involved in the study, according to a news release.
The idea that autistic brains have more synapses isn't new. Guomei Tang, PhD, and colleagues decided to use brain samples to test the hypothesis. They examined brains of children who had died from other causes. Brain samples were derived from both autistic and non-autistic children.
"It's the first time that anyone has looked for, and seen, a lack of pruning during development of children with autism," said David Sulzer, PhD, professor of neurobiology in the Departments of Psychiatry, Neurology, and Pharmacology at CUMC. "Although lower numbers of synapses in some brain areas have been detected in brains from older patients and in mice with autistic-like behaviors."
The team found that the brains of people with autism weren't undergoing autophagy. Usually, cells in brains 'eat' their own damaged parts. But, this process wasn't as efficient in the brains of autism patients as it was in other people.
Scientists even traced why the process was being inhibited. They found that in mice models, high levels of a protein called mTOR leads to a decrease in self-killing abilities of neurons.
"While people usually think of learning as requiring formation of new synapses," Dr. Sulzer said in a news release; further adding: "The removal of inappropriate synapses may be just as important."
The team even showed that rapamycin, a drug that inhibits mTOR, can increase synaptic pruning in mice.
According to the researchers, hundreds of genes have been linked to autism, yet they found that higher activity of a gene that codes for mTOR was linked to autism-like behavior in mice models. The research suggests that lack of synaptic pruning is an essential part of symptoms of autism.
The study is published in the journal Neuron.
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