Envisioning a Bright Future: NMN Supports Eye Health and Protects Retinal Cells From Senescence
In the hierarchy of our five senses—sight, hearing, touch, taste, and smell—many people agree that their eyesight is the most vital and valued. Researchers have studied the value of vision, finding in one study that people chose to have just 4.6 years of perfect health rather than go ten years without sight. As we age, vision impairment severely impacts older adults’ quality of life, mobility, mental health, sociability, and independence. And with over 15% of Americans experiencing vision loss once they reach their mid-70s, finding ways to mitigate this decline is crucial.
One such way may be with the compound NMN (nicotinamide mononucleotide), a precursor to our cells’ most essential molecule—NAD+. Without adequate NAD+ activity, the function of cells in our eyes—and everywhere else in the body—declines, leading to vision problems and eye disorders. Supplementing with NMN may support eye health with age, which researchers from Tongji University in Shanghai, China, showed in a recent study published in Oxidative Medicine and Cellular Longevity. In this research, Ren and colleagues exhibit how NMN protects eye cells from age-related dysfunction, damage, and inflammation that commonly precedes vision loss, providing hope for the millions of people currently suffering from blindness or impaired sight.
The ABCs of RPE
One eye region that is essential for vision and is affected by aging is the retinal pigment epithelium (RPE), a single layer of cells arranged at the outermost layer of the retina. The RPE is necessary for maintaining photoreceptor cells, as it is rich in pigment particles that absorb light and protect the sensitive retinal tissue against oxidation. The RPE also clears out dead cells and debris, modulates the immune system in the eye, and nourishes retinal tissue.
With age, the RPE is less able to perform these functions, causing a buildup of dysfunctional or toxic molecules that cannot be effectively removed. Aged RPE cells tend to exhibit significant loss of NAD+ activity, DNA damage, increased oxidative compounds, and senescence—the accumulation of cells that have undergone permanent growth arrest but remain in the body and cause inflammation.
Researchers like Ren and colleagues speculate that targeting cell senescence may be able to mitigate damage to the RPE and subsequent vision loss—and NMN is a promising candidate for doing so.
NMN Supports Vision By Slashing Senescence
In this study, the Shanghai-based research team induced senescence in RPE cells by adding an oxidizing compound called sodium iodate. These cells developed abnormal mitochondria in both shape and function, had reductions in ATP (energy) and NAD+ levels, and exhibited high activity of senescence-related cell markers.
However, pretreating the cells with NMN before attempting to induce senescence successfully amelioriated these cellular issues. Three senescence biomarkers had significantly reduced activity following NMN pretreatment, and the number of cells with DNA damage was reduced by half. NMN also protected RPE cells from oxidative damage and mitochondrial dysfunction.
The researchers then wanted to see if these results translated to animals, testing the effects of NMN in mice. When mice were pretreated with NMN, the animals had a restoration of NAD+ levels and suppression of cellular senescence in the RPE. The NMN-treated mice also had normalized RPE layer structure and mitochondrial shape and function.
They also discovered that the protein Sirt1 was essential for NMN’s beneficial effects. Sirt1 is a protein in the sirtuin family—often dubbed “longevity genes”—that relies on NAD+ to function properly. When Ren and colleagues inhibited Sirt1 activity in the RPE cells, NMN did not have the same senescence-suppressing effects. However, overactivation of Sirt1 was also detrimental, causing excess RPE cell death, indicating that a moderate and undisturbed level of Sirt1 function is best.
Things Are Looking Up With NMN
As with all cells in the body, those in the retinal pigment epithelium have declining NAD+ levels with age, correlating with cell senescence, DNA damage, and oxidative stress. In this study, researchers found that supplemental NMN supported eye health by mitigating cellular senescence and stabilizing mitochondrial function in the RPE—in both in vitro and in vivo models.
The authors conclude, “Our results showed that RPE senescence was mainly mediated by mitochondrial dysfunction. Moreover, we showed that NMN supplementation replenished the NAD+ levels in RPE cells and ameliorated RPE senescence and senescence-associated retinal inflammation.”
While we don’t yet have studies looking at humans, NMN, and vision loss, researchers envision a bright future on this topic.
Enoch J, McDonald L, Jones L, Jones PR, Crabb DP. Evaluating Whether Sight Is the Most Valued Sense. JAMA Ophthalmol. 2019;137(11):1317-1320. doi:10.1001/jamaophthalmol.2019.3537
Ren C, Hu C, Wu Y, et al. Nicotinamide Mononucleotide Ameliorates Cellular Senescence and Inflammation Caused by Sodium Iodate in RPE. Oxid Med Cell Longev. 2022;2022:5961123. Published 2022 Jul 18. doi:10.1155/2022/5961123