Nicotinamide mononucleotide (NMN) improved photoreceptor cell survival by increasing cellular health-promoting and antioxidant enzyme levels.
Age-related eye disorders, such as age-related macular degeneration, diabetic retinopathy, and retinal detachment, often lead to severe visual impairment and irreversible vision loss. These disorders all feature degraded photoreceptors, the light-responsive cells in the eye, which separate from a cell layer that nourishes visual cells called the retinal pigment epithelium. This separation induces cell death, cell stress from harmful oxygen-containing molecules (oxidative stress), and inflammation. However, no current pharmaceutical approach can treat this photoreceptor degeneration.
Recently, Vavvas and colleagues from Harvard Medical School published research in Aging showing that nicotinamide mononucleotide (NMN) administration protects photoreceptors after retinal detachment and oxidative stress injury. The study indicated that NMN’s protective effects stem from reducing cell death, suppressing eye inflammation, and increasing levels of antioxidants that combat oxidative stress in mouse eyes. Further results showed increased activity of an enzyme—SIRT1—mediated these protective effects. “Taken together, our results suggest a potential therapeutic value of NMN administration in treating photoreceptor degeneration in clinical settings,” said the researchers in their article.