New research shows how the novel drug QNZ-46 can help to lessen the effects of excess release of glutamate in the brain – the main cause of brain injury in stroke.
Published in Nature Communications, the study shows how identifying the source of damaging glutamate in stroke leads to discovery of brain protection with QNZ-46, a novel form of preventative treatment with clinical potential.
Existing studies show that restricted blood supply promotes the excess release of glutamate. The glutamate binds to receptors, over-stimulating them and leading to the break-down of myelin – the protective sheath around the nerve fibre (axon).
Previous studies had focused on the brain’s grey matter – the area where all of the synapses operate. Now the new study focuses on white matter – the part of the brain the connects all of the grey matter together – and demonstrates that the glutamate release from axons themselves contributes to damaging myelin.
The study, led by Professor Robert Fern at the Plymouth University Peninsula Schools of Medicine and Dentistry (PUPSMD), is the first direct comparison of vesicular fusion within different cellular components in white matter, and it reveals extensive fusion in axons – a mechanism previously thought to be absent from white matter.
The findings support a rational approach toward a low-impact prophylactic therapy, such as QNZ-46, to protect patients at risk of stroke and other forms of excitotoxic injury (injury caused by excess glutamate).
As stroke is the second leading cause of disability and early death in the UK, Professor Fern, part of the University’s Institute of Translational and Stratified Medicine, explains the significance of the findings.
