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article imageAltering neurons improves autism in mice

By Tim Sandle     Aug 30, 2014 in Science
Fixing impaired neurons appears to ease the symptoms of autism in laboratory studies on mice, where mice have the disorder. This is according to a new study published in the journal Neuron.
As a child's brain develops there is a trimming back the excess synapses among neurons. This process continues through to adolescence. Previous studies have suggested that this process, and the resultant synapse structure and density might be abnormal in people with autism and in animal models of the disorder.
Autism is a disorder of neural development characterized by impaired social interaction and verbal and non-verbal communication, and by restricted, repetitive or stereotyped behavior. The diagnostic criteria require that symptoms become apparent before a child is three years old.
A new study has found a link between autism and defects in synaptic pruning in humans. The study additionally demonstrates that repairing broken pruning mechanisms can improve autism symptoms in a mouse model.
With the study, The New York Times summarizes, researchers treated the mice with rapamycin, an immunosuppressant that inhibits a protein in the brain called mTOR. The researchers showed that an over activation of mTOR is responsible for the poor synaptic pruning in the mouse model. The researchers then found that they could treat with rapamycin and restore behavior and restore the pruning.
David Sulzer, a neurobiologist at Columbia University Medical Center who led the study, succinctly told The Washington Post: "We were able to treat mice after the disease had appeared."
Although the results are encouraging, further studies are required and data from a mouse model does not necessarily translate into success in people.
The research has appeared in the journal Neuron and it is headed "Loss of mTOR-Dependent Macroautophagy Causes Autistic-like Synaptic Pruning Deficits".
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