Mitochondrial dysfunction in neonatal brain injury
Neonatal hypoxic-ischaemia at term results in life-long consequences for those infants severely affected. The gold standard treatment, therapeutic hypothermia, provides proof-of-concept that post-injury intervention can be effective. However hypothermia is not universally successful and there is an urgent need for synergistic therapies. Mitochondrial dysfunction lies at the centre of the development of neonatal brain injury following hypoxic-ischaemic insult. Not only is mitochondrial dysfunction key in triggering apoptotic cell death but in vivo studies of hypoxic-ischaemia in rodents and in vitro oxygen/glucose deprivation have identified perturbations in mitochondrial dynamics affecting fission, fusion and mitophagy. In particular, the integrity of the mitochondrial fusion protein, Optic Atrophy (OPA)1 appears significantly vulnerable to such insult. Our current research focusses on mechanisms underlying impaired mitochondrial fission and fusion in order to develop strategies for maintaining mitochondrial function, ultimately providing additional neuroprotection for infants following birth asphyxia, where therapeutic hypothermia alone is inadequate.
Date: 8 March 2019, 11:00 (Friday, 8th week, Hilary 2019)
Venue: Sherrington Building, off Parks Road OX1 3PT
Venue Details: Small Lecture Theatre
Speaker: Dr Claire Thorton (King’s College London.)
Organising department: Department of Physiology, Anatomy and Genetics (DPAG)
Organiser: Professor Zoltan Molnar (DPAG, University of Oxford)
Organiser contact email address: zoltan.molnar@dpag.ox.ac.uk
Host: Professor Zoltan Molnar (DPAG, University of Oxford)
Part of: Neuroscience Theme Guest Speakers (DPAG)
Booking required?: Not required
Audience: Members of the University only
Editor: Talitha Smith