Vision depends on photoreceptors in our eye for light transduction. Photoreceptor death is the endpoint of many blinding diseases.
Photoreceptors make up a significant portion of the neurosensory retina, one of the most metabolically active tissues in the body (Ames et al., 1992, Kooragayala et al., 2015, Okawa et al., 2008).
In addition, these receptors have a tremendous metabolic demand and experience significant light-induced oxidative stress due to their role in light transduction( Fu and Yau, 2007, Yau and Hardie, 2009).
Because of their role in light transduction, photoreceptor death leads to blindness.
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WHY DOES THIS HAPPEN?
When we age, the level of NAD+ in our body decreases, leading to metabolic dysfunction and, eventually, photoreceptor death.
Retinal NAD+ (nicotinamide adenine dinucleotide) deficiency is an age-related disease.
It consists of retinal dysfunction, including light-induced degeneration, and streptozotocin-induced diabetic retinopathy.
Identifying treatment strategies to prevent this disease is imperative.
NAD+ has been shown to be important in many biological processes, including metabolism, circadian rhythms, and aging. This is because NAD+ is an essential coenzyme, functioning as an electron carrier in glycolysis and the Krebs cycle.
In fact, NAD+ biosynthesis plays an important role in photoreceptor function and survival.
Researchers identified that rode or cone photoreceptor-specific deletion of NAMPT (nicotinamide phosphoribosyltransferase), the rate-limiting enzyme in NAD+ synthesis, caused retinal degeneration.
They studied the role of NAMPT-mediated NAD+ biosynthesis in photoreceptor survival and vision.
The results are impressive and show the importance of NAD+ in retinal degeneration and age-related retinal dysfunction.
This leads to the possibility of using NAD+ intermediates ( NMN, NR) to protect against retinal degeneration.
For more details and to read the full study, visit the link below: