We aim to understand how synaptic dysfunction underlies seizure activity in humans.
Epileptic seizures are caused by imbalances in the brain leading to over excitement of particular cells. Through our pre-clinical research projects we aim to understand what causes this over excitement in order to discover effective treatments for different types of epilepsy.
Our pre-clinical research feeds directly into the clinical research carried out at the Centre. All MMEC pre-clinical projects adhere to University and NC3R guidelines. For more information please see: www.nc3rs.org.uk and www.ed.ac.uk/research/animal-research.
Our aim is to gain greater understanding of the disease and to use that knowledge to develop better preventative measures and treatments for children with epilepsy. Professor Sir John Savill, Head of the College of Medicine and Veterinary Medicine
Brain cells (neurones) communicate at junctions called synapses. Communication occurs when one neurone releases chemical neurotransmitters that are recognised by the other neurone at the synapse. These neurotransmitters can either “excite” their synaptic partner, making them communicate more, or they “inhibit” them, making them less likely to talk.
Epileptic seizures can occur when there is an imbalance in the balance of excitation and inhibition at synapses, making neurones “too talkative”.
This imbalance can occur through either dysfunctional neurotransmitter release, or errors in recognising and interpreting the neurotransmitter signal. Understanding this phenomenon is a hugely complex task, since the human brain has on average 100,000,000,000 neurones and each neurone has 10,000 synapses!
We aim to understand how synaptic dysfunction underlies seizure activity in humans, via use of a series of pre-clinical epilepsy model systems of increasing complexity.
We are currently establishing a strong research base, which will inform provide key information for future translational and clinical studies into both the cause and treatment of epilepsy.
To understand how
1) altered neurotransmitter release may contribute towards refractory epilepsy and;
2) how modulation of specific neurotransmitter release pathways may be a therapeutic avenue for controlling seizure activity.
To understand how synapses develop in the cortex of a preclinical model of childhood absence epilepsy.
To understand how recently identified mutations in the gene eEF1A2 contribute towards the development of epilepsy.
To understand how changes in the inhibitory neurones during neurodegenerative conditions such as Alzheimer’s disease can lead to epilepsy.
To translate information from studies of intellectual disability regarding synaptic malfunction into viable treatment strategies for epileptic seizure.
To understand how defects in the assembly of synapses due to mutations in the gene leucine-rich glioma inactivated glycoprotein contribute towards the development of epilepsy.