Neuroprotection in Glaucoma: NAD+/NADH Redox State As a Potential Biomarker and Therapeutic Target
cells Review Neuroprotection in Glaucoma: NAD+/NADH Redox State as a Potential Biomarker and Therapeutic Target Bledi Petriti 1,2, Pete A. Williams 3 , Gerassimos Lascaratos 4, Kai-Yin Chau 2 and David F. Garway-Heath 1,* 1 NIHR Biomedical Research Centre, Moorfields Eye Hospital and UCL Institute of Ophthalmology, London EC1V 9EL, UK; b.petriti@ucl.ac.uk 2 Department of Clinical & Movement Neurosciences, UCL Queens Square Institute of Neurology, London NW3 2PF, UK; k.chau@ucl.ac.uk 3 Department of Clinical Neuroscience, Division of Eye and Vision, St. Erik Eye Hospital, Karolinska Institutet, 171 64 Stockholm, Sweden; Pete.williams@ki.se 4 King’s College Hospital NHS Foundation Trust, London and King’s College London, London SE5 9RS, UK; gerassimos.lascaratos@nhs.net * Correspondence: d.garwayheath@nhs.net Abstract: Glaucoma is the leading cause of irreversible blindness worldwide. Its prevalence and incidence increase exponentially with age and the level of intraocular pressure (IOP). IOP reduction is currently the only therapeutic modality shown to slow glaucoma progression. However, patients still lose vision despite best treatment, suggesting that other factors confer susceptibility. Several studies indicate that mitochondrial function may underlie both susceptibility and resistance to developing glaucoma. Mitochondria meet high energy demand, in the form of ATP, that is required for the maintenance of optimum retinal ganglion cell (RGC) function. Reduced nicotinamide adenine Citation: Petriti, B.; Williams, P.A.; dinucleotide (NAD+) levels have been closely correlated to mitochondrial dysfunction and have Lascaratos, G.; Chau, K.-Y.; been implicated in several neurodegenerative diseases including glaucoma. NAD+ is at the centre Garway-Heath, D.F.
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