The relevance of poor glycaemic control to stroke outcome

Diabetic patients suffer an increased risk of stroke. One potential contributory mechanism may be that poor glycaemic control interferes with neuroprotective mechanisms. My host laboratory has developed a novel microfluidic model to study neurotoxicity and counterbalancing neuroprotective mechanisms in networks and discovered a new fast-acting neuroprotective activity operating at the level of the network. Preliminary evidence indicates that this network cooperation is compromised by hypoglycaemia, but the mechanism is unknown. This project provides a unique opportunity to investigate how neuronal responses (morphological changes, network functionality and the recruitment of neuroprotection) are compromised by altered glucose availability. Using this novel, in vitro microfluidic model, a greater scientific understanding of these processes can be rapidly developed. Potential therapeutic/neuroprotective approaches will then be validated using an in vivo middle cerebral artery occlusion (MCAO) model of stroke in both normal and diabetic rodents.