Researchers from University College London and Moorfields Eye Hospital have identified biomarkers that predict whether glaucoma patients are at higher risk of continued vision loss following conventional treatment.
More than 300,000 people are estimated to be living with glaucoma in Australia and it is the leading cause of irreversible blindness worldwide. Despite advancements in glaucoma therapy, some patients continue to lose their sight following treatment.
The study published in Nature Medicine, explored if mitochondrial function, measured in white blood cells, is associated with the rate at which glaucoma patients lose vision.
The researchers assessed 139 participants who were already receiving treatment to lower intraocular pressure (IOP) and 50 healthy people acting as a control group.
They measured how well cells in the blood use oxygen, how much vision was lost over time and nicotinamide adenine dinucleotide (NAD) levels. NAD is a molecule in the body that helps cells produce energy and is made from vitamin B3 in the diet.
Firstly, the researchers discovered that certain cells in the blood, known as peripheral blood mononuclear cells, use oxygen differently in people with glaucoma.
The team measured how much oxygen these cells use and found that people whose blood cells used less oxygen tended to lose their vision faster, even if they were being treated to lower IOP. This measurement explained 13% of the differences in how fast patients lost vision.
Additionally, people with glaucoma were found to have lower levels of NAD in their blood cells compared to people without glaucoma. These lower NAD levels were linked to the lower oxygen use in the blood cells.
“This study provides evidence of the strong association between mitochondrial respiratory activity and the rate of disease progression in glaucoma,” the study authors said.
“The findings have practical implications for clinical decision-making. Low oxygen consumption rate (OCR) and/or NAD may identify patients at risk of faster progression, informing personalised treatment strategies and, if shown to be causative, offering the potential for mitochondria-targeted therapies.”
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