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Review

Neuroprotection in Glaucoma: NAD+/NADH Redox State as a Potential Biomarker and Therapeutic Target

1
NIHR Biomedical Research Centre, Moorfields Eye Hospital and UCL Institute of Ophthalmology, London EC1V 9EL, UK
2
Department of Clinical & Movement Neurosciences, UCL Queens Square Institute of Neurology, London NW3 2PF, UK
3
Department of Clinical Neuroscience, Division of Eye and Vision, St. Erik Eye Hospital, Karolinska Institutet, 171 64 Stockholm, Sweden
4
King’s College Hospital NHS Foundation Trust, London and King’s College London, London SE5 9RS, UK
*
Author to whom correspondence should be addressed.
Academic Editors: Stanislav I. Tomarev and Ben Mead
Cells 2021, 10(6), 1402; https://doi.org/10.3390/cells10061402
Received: 30 April 2021 / Revised: 24 May 2021 / Accepted: 27 May 2021 / Published: 5 June 2021
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 dinucleotide (NAD+) levels have been closely correlated to mitochondrial dysfunction and have been implicated in several neurodegenerative diseases including glaucoma. NAD+ is at the centre of various metabolic reactions culminating in ATP production—essential for RGC function. In this review we present various pathways that influence the NAD+(H) redox state, affecting mitochondrial function and making RGCs susceptible to degeneration. Such disruptions of the NAD+(H) redox state are generalised and not solely induced in RGCs because of high IOP. This places the NAD+(H) redox state as a potential systemic biomarker for glaucoma susceptibility and progression; a hypothesis which may be tested in clinical trials and then translated to clinical practice. View Full-Text
Keywords: glaucoma; mitochondrial dysfunction; retinal ganglion cell (RGC); nicotinamide adenine dinucleotide (NAD+); NAD+/NADH redox state; ATP; neurodegenerative disease glaucoma; mitochondrial dysfunction; retinal ganglion cell (RGC); nicotinamide adenine dinucleotide (NAD+); NAD+/NADH redox state; ATP; neurodegenerative disease
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MDPI and ACS Style

Petriti, B.; Williams, P.A.; Lascaratos, G.; Chau, K.-Y.; Garway-Heath, D.F. Neuroprotection in Glaucoma: NAD+/NADH Redox State as a Potential Biomarker and Therapeutic Target. Cells 2021, 10, 1402. https://doi.org/10.3390/cells10061402

AMA Style

Petriti B, Williams PA, Lascaratos G, Chau K-Y, Garway-Heath DF. Neuroprotection in Glaucoma: NAD+/NADH Redox State as a Potential Biomarker and Therapeutic Target. Cells. 2021; 10(6):1402. https://doi.org/10.3390/cells10061402

Chicago/Turabian Style

Petriti, Bledi, Pete A. Williams, Gerassimos Lascaratos, Kai-Yin Chau, and David F. Garway-Heath. 2021. "Neuroprotection in Glaucoma: NAD+/NADH Redox State as a Potential Biomarker and Therapeutic Target" Cells 10, no. 6: 1402. https://doi.org/10.3390/cells10061402

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