This experiment examined the causes of loss of mitochondrial function with age.

Specifically, the experiment tested the influence of the gene SIRT-1s expression on the
metabolism of mice and the effects of Nicotinamide mononucleotide (NMN) - a precursor of
NAD+. The goal of the experiment was to determine if the introduction of NMN would increase
the mouses production of NAD+ and improve the metabolism of the mice that received it. Mice
who were not given the NMN precursor were found to have declining levels of NAD+, ATP, and
COX as they aged. SIRT-1 is a gene that produces a protein called sirtuin-1 and influences the
regulation of NAD+ in the cell (it is regulated by the availability of intracellular NAD+). As the
function of NAD+ is to transport electrons during cellular respiration (the generation of ATP
from glucose), its presence is essential to the overall efficiency of the metabolism.
When an organisms metabolism is efficient and coupled with caloric restriction to reduce
the production of free radicals free electrons associated with molecular damage and increased
mortality it appears to have the potential to increase the lifespan of said organism. During the
experiment, after knocking out SIRT-1 the presence of COX and ATP decreased in the mice
resulting in the metabolisms of the mice becoming less efficient (they resembled the metabolisms
of older mice). This implies that the presence of SIRT-1 is essential to maintaining metabolic
function. After receiving the NMN precursor, there was a marked increase in the NAD+, ATP,
and COX levels in the mice. The study found that there was a correlation between the expression
of the SIRT-1 gene and the metabolic efficiency of the tested mice.
According to the study, the treatment of old mice with NMN reversed all of these
biochemical aspects of aging and switched gastrocnemius muscle to a more oxidative fiber type
(Gomes) showing that the supplement does positively impact the metabolism of the treated
mices skeletal muscle. While the experiment did, in fact, show that the older mices declining
metabolic function was reversed after being given the NMN precursor, the tissue that was tested
in the mice was skeletal tissue, and is not the sole variable in the lifespan of mammals.
Furthermore, the study concluded by stating 1 week of treatment might not be sufficient to
reverse whole-organism aging and that longer treatments might be required since there was no
observable improvement in muscle strength (Gomes). Therefore, it is not possible to
conclusively state that the NMN supplement extended the mices lifespan significantly and did
not merely create well-muscled elderly mice.
I personally believe that the information gleaned from this experiment is valuable and
should be studied further - particularly the genetic determinants of metabolism. There are
certainly effective applications for this supplement, but the same can be said about blood doping.
Since mice and humans have very similar genomes, the applications of this supplement should
extend across species. The National Human Genome Research Institute states that of the 4,000
genes that have been studied, less than 10 are found in one species but not the other (Why
Mouse Matters). Assuming that researchers can find the equivalent SIRT-1 gene in humans, I
dont see why the NMN precursor applied to humans wouldnt produce similar results to those of
the mice that were tested in this experiment.
 Works Cited:
Gomes, A., et al. (2014). Declining NAD+ Induces a Pseudohypoxic State Disrupting
Nuclear-Mitochondrial Communication during Aging. Bethesda, National Institute of
Health.
(2000). Why Mouse Matters. Bethesda, National Human Genome Research Institute.