Researchers from UCL and Moorfields Eye Hospital have identified potential markers in the blood that could change the treatment of glaucoma, a leading cause of irreversible blindness worldwide
Glaucoma affects over 700,000 people in the UK alone and is primarily characterised by the gradual death of retinal ganglion cells, essential for vision.
Current treatments for glaucoma
Currently, treatments focus on reducing intraocular pressure, a key risk factor alongside advancing age. Despite these treatments, some patients continue to experience vision loss.
The study, published in Nature Medicine, investigated whether mitochondrial function in white blood cells could help us understand why certain patients fare worse than others.
Mitochondria, often referred to as the ‘batteries’ of cells, produce energy crucial for cellular function, particularly in energy-demanding tissues like the eye. The team assessed 139 patients already receiving standard intraocular pressure-lowering treatments and compared them to 50 healthy individuals. They specifically examined how efficiently peripheral blood mononuclear cells (PBMCs) utilised oxygen and measured levels of nicotinamide adenine dinucleotide (NAD), a molecule essential for energy production derived from vitamin B3.
Who is at higher risk of vision loss?
The findings revealed significant differences between patients with glaucoma and healthy controls. Glaucoma patients exhibited altered oxygen utilisation by their PBMCs, with those showing lower oxygen usage experiencing faster rates of vision loss, independent of intraocular pressure levels. This discovery accounted for 13% of the variation in vision loss rates among patients.
The study also highlighted lower levels of NAD in blood cells of glaucoma patients compared to healthy individuals. These lower NAD levels were closely associated with impaired oxygen utilisation in PBMCs, suggesting a potential link between mitochondrial dysfunction and accelerated vision loss.
Professor David Garway-Heath, senior author of the study from UCL Institute of Ophthalmology and Moorfields Eye Hospital, emphasised the clinical implications of these findings. If implemented as a diagnostic tool, assessments of PBMC mitochondrial function and NAD levels could help clinicians predict which patients are at higher risk of ongoing vision loss. This predictive capability would enable targeted monitoring and intensified treatment strategies for high-risk individuals.
The study was made possible with support from several organisations including Santen SenSyT, Fight for Sight, Glaucoma UK, Rosetrees Trust, Alcon Research Institute, and the NIHR Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology.
By incorporating these blood-based markers into clinical practice, healthcare providers could potentially improve outcomes by identifying and treating those most vulnerable to progressive vision loss. Future research aims to validate these findings in larger patient cohorts and explore therapeutic interventions targeting mitochondrial function to further enhance patient care.
