OxTalks will soon move to the new Halo platform and will become 'Oxford Events.' There will be a need for an OxTalks freeze. This was previously planned for Friday 14th November – a new date will be shared as soon as it is available (full details will be available on the Staff Gateway).
In the meantime, the OxTalks site will remain active and events will continue to be published.
If staff have any questions about the Oxford Events launch, please contact halo@digital.ox.ac.uk
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.
