University of Washington: NMN is essential for maintaining vision in old age

Release Date:2024-03-06

As people get older, they are prone to a variety of vision diseases, such as age-related macular degeneration, which causes the gradual death of photoreceptor cells, resulting in loss of vision.

 

In 2016, the research team of Professor Shinichiro Imai at the University of Washington found that lack of NMN (niacinamide mononucleotide) caused the death of rod and cone cells in mice, which significantly reduced the vision of mice; Treating mice with NMN reversed this and restored the mice's vision. The study was published in the journal Cell Reports.

 

In the experiment, the researchers first knocked out the gene expressing the Nampt protein in mouse rod cells by gene editing means, which led to a significant reduction in NMN levels in mouse rod cells.

 

After 6 weeks of normal feeding, the researchers found that mice lacking rod cell NMN (NAMPT-rod /-rod) showed a significant decrease in visual acuity and performance on electroretinogram (ERG) tests compared to control mice (NamptF/F).

 

At the same time, the fundus images of mice lacking rod cell NMN were more cloudy, and a series of symptoms such as retinal decomposition and optic nerve decline occurred. It is proved that rod NMN plays a crucial role in maintaining the vision of mice.

 

Next, the researchers knocked down the gene for the Nampt protein on the mouse cone cells, and similar results showed a significant reduction in vision. This once again verified the important role of NMN levels in maintaining the function of photoreceptor cells in mice.

 

After confirming the damage to vision caused by the lack of NMN, the researchers tried to treat mice with NMN to restore their vision. The results showed that after receiving 300mg/kg of NMN intraperitoneal injection (approximately 1.35g in humans) for 6 consecutive days, mice lacking either rod NMN or cone NMN showed significant visual improvement.

 

In conclusion, this study confirmed the key role of NMN in protecting visual health by artificially reducing and restoring NMN levels in mouse photoreceptor cells. And as the researchers said, "because the NMN synthesis pathway is ubiquitous in all kinds of neurons, and supplementing NMN may have a protective effect on nerves, this study also provides a new idea for the treatment of other neurodegenerative diseases, such as brain atrophy and Alzheimer's disease."


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