Research, conducted at the Jackson Laboratory, Bar Harbor, Maine, has reported that therapeutic use of vitamin B3 was successful in blocking the progression of glaucoma in 93% of eyes tested. In addition, a higher dose of the same molecule was also able to protect against both intraocular pressure (IOP) elevation and neural vulnerability. Such a simple therapeutic approach may hold considerable potential for glaucoma treatment.
An estimated 70 million people suffer globally from glaucoma, in respect of which high IOP and increasing age are significant risk factors. Research however has also indicated that mitochondrial dysfunction may play a role in the disease pathology. Analysis conducted on models of glaucoma has shown that early decreases in metabolites required for healthy mitochondrial functioning, specifically nicotinamide adenine dinucleotide (NAD+), and the reduced form of NAD+, were associated with increasing age and disease. Age dependent declines of NAD+ may cause retinal ganglion cells to become more sensitive to cellular stresses, shunting them towards fatty acid metabolism with a concomitant increase in free radicals and reactive oxygen species (ROS).
The recent US research sought to supplement the diet of mice models with oral vitamin B3, otherwise known as nicotinamide (NAM), a precursor of NAD. Vitamin B3 supplementation was thus aimed at increasing the levels of NAD to prevent glaucomatous changes through rendering retinal ganglion cells more resistant to cellular stresses. At an initial dose of 550mg/kg per day, administered in drinking water, the experimental therapy resulted in the prevention of declining NAD levels. The supplement appeared to be protective prophylactically, in addition to significantly reducing the incidence of optic nerve degeneration, retinal nerve fibre thinning and had a protective effect on visual function. A higher does of 2,000mg/kg per day appeared to eliminate optic nerve damage in 93% of the eyes tested. According to the researchers, “[T]he degree of protection afforded by administering this single molecule is unprecedented and unanticipated.” The research indicated that the higher dosage of NAM not only protected retinal ganglion cells, but also had a clear neuroprotective effect through lessening the degree of IOP elevation. The researchers additionally explored the potential for using gene therapy through over expressing Nmnat1, a enzyme critical to the production of NAD+. Combining a gene therapy approach with low dosage vitamin B3 supplementation resulted in a 4-fold decreased risk of developing glaucoma.