Management of Autism Spectrum Disorders, ASD has received a boost as researchers from McGill University and the University of Montreal have identified a crucial link between protein synthesis and autism spectrum disorders, which can bolster new therapeutic avenues.
ASD encompass a wide array of neurodevelopmental diseases that affect three areas of behaviour: social interactions, communication and repetitive interests or behaviours. According to the U.S.-based Centers for Disease Control and Prevention, 1 in 88 children suffer from ASD, and the disorder is reported to occur in all racial, ethnic, and socioeconomic groups. ASDs are almost five times more common among boys (1 in 54) than among girls (1 in 252).
In Nigeria, there is no accurate statistics yet but experts say about 308, 000 Nigeria children under the age of 14 may be suffering from the disorder.
The new study in mice found that abnormally high synthesis of a group of neuronal proteins called neuroligins results in symptoms similar to those diagnosed in ASD. The study also revealed that autism-like behaviours can be rectified in adult mice with compounds inhibiting protein synthesis, or with gene-therapy targeting neuroligins.
On the study published in the journal Nature, Prof. Nahum Sonenberg, from McGill’s Dept. of Biochemistry, Faculty of Medicine said: My laboratory is dedicated to elucidating the role of dysregulated protein synthesis in cancer etiology. However, our team was surprised to discover that similar mechanisms may be implicated in the development of ASD.”
“We used a mouse model in which a key gene controlling initiation of protein synthesis was deleted. In these mice, production of neuroligins was increased. Neuroligins are important for the formation and regulation of connections known as synapses between neuronal cells in the brain and essential for the maintenance of the balance in the transmission of information from neuron to neuron,” he explained.
According to the Lead author, Christos Gkogkas, “Since the discovery of neuroligin mutations in individuals with ASD in 2003, the precise molecular mechanisms implicated remain unknown.”
“Our work is the first to link translational control of neuroligins with altered synaptic function and autism-like behaviors in mice. The key is that we achieved reversal of ASD-like symptoms in adult mice. Firstly, we used compounds, which were previously developed for cancer treatment, to reduce protein synthesis. Secondly, we used non-replicating viruses as vehicles to put a break on exaggerated synthesis of neuroligins.”