image: Protective effects of delayed NMN administration to retinal detachment (RD). (A) A flow chart for the in vivo experiments. (B-E) Delayed NMN administration still have protective effect to outer nuclear layer (ONL) thickness 7 days post RD. N = 3 to 4 eyes per group. Scale bar=50 μm. (C-F) Reduced number of CD11b+ infiltrating macrophages (red) in delayed NMN-treated groups compared to vehicle. N = 3 eyes per group. Scale bar: 100 μm. (D-G) No significance was found between NMN and vehicle treated retinas of the GFAP (green). N = 3 eyes per group. Scale bar: 50 μm. Statistical significance was analyzed with the unpaired Student's t-test. *p<0.05. **p<0.01. ***p<0.001. Data are mean ± SEM. view more
Credit: Correspondence to: Demetrios G. Vavvas email: demetrios_vavvas@meei.harvard.edu
Aging-US published "Neuroprotective effects and mechanisms of action of nicotinamide mononucleotide (NMN) in a photoreceptor degenerative model of retinal detachment" which reported that here, the authors investigated nicotinamide mononucleotide, a precursor of nicotinamide adenine dinucleotide, in a retinal detachment induced photoreceptor degeneration.
NMN administration after RD resulted in a significant reduction of TUNEL photoreceptors, CD11b macrophages, and GFAP labeled glial activation; a normalization of protein carbonyl content, and a preservation of the outer nuclear layer thickness.
NMN administration significantly increased NAD levels, SIRT1 protein expression, and heme oxygenase-1 expression.
Delayed NMN administration still exerted protective effects after RD.
This Aging-US article concludes that NMN administration exerts neuroprotective effects on photoreceptors after RD and oxidative injury, suggesting a therapeutic avenue to treating photoreceptor degeneration.
Dr. Demetrios G. Vavvas from Harvard Medical School said, "Major photoreceptor degenerative diseases are primarily age-related eye disorders, leading to severe vision impairment or irreversible vision loss."
Despite distinct differences between these diseases, the separation of photoreceptors from the underlying retinal pigment epithelium or a loss of functional RPE, and eventual photoreceptor death is common to all of them.
Since photoreceptors are highly metabolic, nutrient deprivation from the separated RPE induces the pathological responses that result in permanent neuronal loss.
Fortunately, the separation of photoreceptors from the RPE can be well-modeled in animals.
To date, however, little is known about the role of NAD when photoreceptors are separated from the RPE and whether the NAD and SIRT1 may play a role in protecting photoreceptors during their separation from the underlying RPE.
The Vavvas Research Team concluded in their Aging-US Priority Research Paper, "our study demonstrates the neuroprotective effects of NMN supplementation in rescuing photoreceptor degeneration after RD. NMN treatment was associated with an increase in NAD+ and SIRT1 levels in the injured retina, leading to anti- apoptotic, anti-inflammatory, and antioxidant effects. The therapeutic effect of NMN may occur at least partially through the activation of SIRT1/HO-1 signaling. These results provide an impetus for studies in larger animals and humans with photoreceptor degeneration in a clinical setting"
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Full Text - https://www.aging-us.com/article/202453/text
Correspondence to: Demetrios G. Vavvas email: demetrios_vavvas@meei.harvard.edu
Keywords: nicotinamide mononucleotide, photoreceptor degeneration, NAD+, SIRT1, neuroprotection
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research as well as topics beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, cancer, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR among others), and approaches to modulating these signaling pathways.
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