A groundbreaking study conducted by UCL and Moorfields Eye Hospital has revealed important indicators in the blood that could foretell the likelihood of glaucoma patients losing vision even after traditional treatment. Glaucoma, a leading cause of irreversible blindness, affects over 700,000 individuals in the UK and countless more worldwide.
This sight-threatening condition arises when retinal ganglion cells, responsible for vision, begin to deteriorate. High intraocular pressure and aging are the primary risk factors for glaucoma. All approved treatments aim to reduce intraocular pressure, but some patients continue to experience vision loss despite undergoing treatment.
In an effort to help medical professionals predict and understand the rate of vision loss, the research, published in Nature Medicine, hypothesized whether mitochondrial function in white blood cells is lower in glaucoma patients in comparison to those without the disease. Furthermore, it investigated whether this function is associated with the vision loss rate in glaucoma patients.
Mitochondria are known as the cells’ ‘powerhouses,’ generating the energy necessary for cellular functions. The eye cells, in particular, require substantial energy. The study evaluated 139 glaucoma patients receiving intraocular pressure-reducing treatment and a control group of 50 healthy individuals.
Parameters such as how effectively blood cells utilized oxygen, vision loss progression, and Nicotinamide Adenine Dinucleotide (NAD) levels were measured. NAD, a vitamin B3-derived molecule, aids in the cells’ energy production.
The researchers found that Peripheral Blood Mononuclear Cells, a certain type of blood cell, consumed oxygen differently in glaucoma patients. They noted that patients whose blood cells utilized less oxygen experienced faster vision loss even when receiving intraocular pressure-lowering treatment. This factor accounted for a 13% variation in the vision loss rate among patients.
Additionally, glaucoma patients exhibited lower NAD levels in their blood cells compared to non-glaucoma individuals. This deficiency correlated with the reduced oxygen usage in blood cells.
Professor David (Ted) Garway-Heath from the UCL Institute of Ophthalmology and Moorfields Eye Hospital, the study’s senior author, suggested that introducing a clinical test for white blood cell mitochondrial function and NAD levels could aid clinicians in identifying patients at a higher risk of continued vision loss. This would enable them to prioritize these patients for more rigorous monitoring and treatment.
He further added that if subsequent research establishes low mitochondrial function or NAD levels as a causative factor for glaucoma, it could pave the way for novel treatments. UCL and Moorfields Eye Hospital are presently spearheading a significant clinical trial, funded by the Medical Research Council and the National Institute for Health and Care Research. The trial aims to determine if high-dose vitamin B3 can enhance mitochondrial function and curb vision loss in glaucoma patients.
The study received support from several organizations, including Santen SenSyT, Fight for Sight, Glaucoma UK, Rosetrees Trust, Alcon Research Institute, and the National Institute for Health and Care Research (NIHR) Biomedical Research Centre at Moorfields Eye Hospital NHS Foundation Trust and UCL Institute of Ophthalmology.
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