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,
*
Citation: 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
Academic Editors: Stanislav
I. Tomarev and Ben Mead
Received: 30 April 2021
Accepted: 27 May 2021
Published: 5 June 2021
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Attribution (CC BY) license (https://
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4.0/).
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
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.
Keywords: glaucoma; mitochondrial dysfunction; retinal ganglion cell (RGC); nicotinamide adenine
dinucleotide (NAD
+
); NAD
+
/NADH redox state; ATP; neurodegenerative disease
1. Introduction
Glaucoma is one of the most common neurodegenerative diseases and the leading
cause of irreversible blindness worldwide. Its prevalence increases with age and affects
~80 million people worldwide, with primary open–angle glaucoma (POAG) being the
most frequent form. Due to the rapid increase in ageing populations worldwide, it is
estimated that the number affected will increase to 111.8 million in 2040 [1]. The number of
hospital related glaucoma visits surpasses one million per year in England and Wales alone,
putting a significant strain on health services [2]. The disease is often associated with fear
of vision loss, consequent social withdrawal, and depression from impaired vision causing
a significant psychological burden to the patient as vision decreases [3]. Thus, glaucoma is
a significant social and economic burden. This underlines the need to prioritise research in
this area and to develop new treatments for glaucoma.
Progressive neurodegeneration of retinal ganglion cells (RGCs; the output neurons of
the retina) and their axons, which make up the optic nerve, is the hallmark of glaucoma.
The optic nerve is particularly sensitive to mitochondrial dysfunction and bioenergetic
Cells 2021, 10, 1402. https://doi.org/10.3390/cells10061402 https://www.mdpi.com/journal/cells