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
Maternally inherited mitochondrial disease are uniquely hard to manage because of a unique feature called heteroplasmy. Mutant and normal mitochondrial DNA (mtDNA) coexist in patients with heteroplasmic mtDNA disease. The load of mutant mtDNA is a key determinant of severity and of the remarkably variable transmission of mutant mtDNA to the offspring. Pre-implantation genetic screening and mitochondrial replacement therapy may enable patients to have healthy offspring.
Mitophagy is a cellular mechanism for recycling damaged mitochondria. It is one of the factors held to reduce the mutant mtDNA that accumulates in patient tissues and underlies progressive symptoms. Nevertheless, whether mitophagy is important in vivo is completely unknown.
We have developed high throughput imaging and shown, for the first time, that mitophagy is commonplace in mitochondrial diseases. We are developing drug modulators of mitophagy both as potential novel treatments for disease and for preventing mutant mtDNA transmission.
