The causes of visual impairment are complex and diverse, but photoreceptor death is the end of many blinding diseases. Photoreceptors form an important part of the neurosensory retina, which is one of the most metabolically active tissues in the body. Studies have shown that multiple mouse models of retinal dysfunction (light-induced degeneration, streptozotocin-induced diabetic retinopathy, and age-related retinal dysfunction) all exhibit early retinal NAD+ deficiency. NAD+ not only performs coenzyme function in each step of the tricarboxylic acid cycle and glycolysis, but also maintains optimal Sirt3 activity. Sirt3 and Sirt5 play important roles in retinal homeostasis. The lack of NAD+ causes a variety of metabolic dysfunctions (such as glycolysis dysfunction and mitochondrial dysfunction) and does not properly respond to metabolic stress, which ultimately leads to photoreceptor death and retinal degeneration. The researchers found that supplementation with nicotinamide mononucleotide
restored normal saccharide function, mitochondrial function, and ability to adapt to metabolic stress, reduced photoreceptor cell death, and significantly improved dark vision and retinal function. The CAS number of NMN
is 1094-61-7. These conclusions support the possibility of using NAD+ intermediate NMN to treat retinal degenerative diseases, define a uniform therapeutic target for ophthalmic degenerative diseases, and provide a powerful therapeutic approach. Since it can be implemented for a variety of diseases with multiple pathogenic mechanisms, the impact of this treatment strategy will be far-reaching once it is successfully implemented.