The Cross-Border Biotech Blog

Biotechnology, Health and Business in Canada, the United States and Worldwide

Friday Science Review: November 30, 2012

John HolyoakeAutism spectrum disorder (ASD) encompasses a range of developmental disorders that effect multiple basic functions including language and socialization. Specific causes of ASD have not been determined, though multiple risk factors have been identified, including genetic components and prenatal complications. Increased neuronal connectivity as a result of dysregulated and overactive synaptic protein expression is, however, proposed to be part of the molecular mechanism.

mTOR has previously been implicated in the observed overactive protein expression, but events downstream of mTOR have not been investigated. It is known that mTOR phosphorylates eukaryotic translation initiation factor 4E-binding proteins (4E-BPs), which are important for suppressing initiation of the translation of mRNA’s and therefore researchers at McGill University and the Université de Montréal investigated the effects of knocking out 4E-BP2 and of overexpressing eukaryotic translation initiation factor 4E (eIF4E). Their paper in Nature shows that both of these perturbations lead to overexpression of neuroligins, a postsynaptic protein class implicated in ASDs. Furthermore, the 4E-BP2 KO mice exhibited autism-like behaviours and had an altered excitatory-inhibitory synaptic balance. Returning neuroligin 1 levels to their normal range restored the synaptic balance, as did pharmacologic inhibition of eIF4E, opening up new avenues to explore for therapeutic interventions in ASDs.

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