On 28th November OxTalks will move to the new Halo platform and will become 'Oxford Events' (full details are available on the Staff Gateway).
There will be an OxTalks freeze beginning on Friday 14th November. This means you will need to publish any of your known events to OxTalks by then as there will be no facility to publish or edit events in that fortnight. During the freeze, all events will be migrated to the new Oxford Events site. It will still be possible to view events on OxTalks during this time.
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Energy metabolism deficits are prevalent in autism spectrum disorder (ASD) and other mental conditions; however, causes of this comorbidity remain a puzzle. Genetic studies strongly implicated Wnt/β-catenin signalling and its effector the TCF7L2 transcription factor in neurodevelopmental disorders, including ASD. On the other hand, TCF7L2 gene variants are the strongest risk factors for type II diabetes. In my presentation, I will show experimental evidence that TCF7L2, in addition to its functions in the metabolic tissues, regulates energy metabolism in the highly interconnected thalamocortical circuit. Furthermore, thalamic deficiency of TCF7L2 causes autism-like behaviours. To explore the potential link between brain energy metabolism and ASD, we fed Tcf7l2-cKO mice with ketogenic diet, which normalised brain energy metabolism and improved social interactions. We propose that ASD can originate from compromised energy metabolism in thalamocortical circuits, and ketogenic diet may ameliorate core ASD symptoms in patients with enhanced aerobic glycolysis.
