Glaucoma is one of the most common causes of visual impairment, affecting 70 million people worldwide. It is characterized by progressive degeneration of the optic nerve, which can lead to loss of peripheral vision and eventual blindness. At the cellular level, there is gradual dysfunction and loss of retinal ganglion cells and their axons, which make up the optic nerve. Most people with glaucoma have elevated intraocular pressure (IOP), and this elevation is a major factor in the development of optic nerve damage. Medications that lower elevated IOP are the mainstay of conventional therapy, and these medications frequently halt or slow the progression of glaucoma. However, some people develop glaucoma despite having normal IOP, and medical therapy that normalizes IOP does not always stop disease progression. Those observations suggest that factors other than increased IOP also contribute to the pathogenesis of glaucoma.

The retina is one of the most metabolically active tissues in the body and, as such, requires an ongoing supply of energy, which is obtained by mitochondrial production of adenosine triphosphate (ATP). The DBA/2J mouse is a genetic strain of mice that spontaneously develops glaucoma. This strain of mice is widely used in research as an animal model of age-related inherited glaucoma. In a study of DBA/2J mice, mitochondrial abnormalities were found in retinal ganglion cells before cellular degeneration was detectable.¹ That finding raises the possibility that impaired mitochondrial energy production renders retinal ganglion cells more susceptible to degeneration and more vulnerable to the adverse effects of increased IOP. If that is true, then supplementing with nutrients that play a role in mitochondrial energy production (such as niacinamide, coenzyme Q10, and magnesium) could be useful for preventing and treating glaucoma.