This correspondence comments on a 10-year real-world observational study (Wong et al.) linking glaucoma subtypes to subsequent neurodegenerative disease risk, arguing that mitochondrial dysfunction deserves greater emphasis as a shared biological mechanism across glaucoma subtypes and related neurodegeneration.
The authors highlight that normal-tension glaucoma (NTG) was the subtype most clearly linked to subsequent Parkinson disease in the index study, and propose mitochondrial dysfunction — including impaired oxidative phosphorylation, defective mitophagy, and mitochondrial DNA variants — as a plausible unifying mechanism connecting glaucoma to neurodegenerative conditions such as Parkinson disease and Alzheimer disease.
This is a commentary with no original data; arguments are hypothesis-generating and based on secondary synthesis of cited studies. The proposed role of mitochondrial dysfunction as a shared susceptibility factor remains unproven and is difficult to test in large database cohorts.
Clinicians managing glaucoma — especially NTG — should be aware of the emerging evidence linking mitochondrial dysfunction to both ocular and central neurodegeneration, though this does not yet change practice. Future studies integrating glaucoma phenotyping with mitochondrial function assessments may clarify whether shared biological pathways underlie these epidemiological associations.
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