Why do we age?

There are species in the animal kingdom that do not age, undying creatures. Can we become one of them?

Reduced capacity for self-renewal and removal of cell waste.

There are three main components that scientist know of so far that has direct links to the aging process. NAD+, senescent cells and stem cells.

Cells are made of hundreds of millions of parts. They’re the structures, machines, messengers, and the catalysts that make reactions happen. All these parts constantly need to be destroyed, cleaned up, and rebuilt. As we age, this process becomes less effective and so parts become crumpled, bunched up, or are removed slower, or they are no longer produced in the quantities we need. One of these parts is NAD+, a coenzyme that tells our cells to look after themselves. The levels of NAD+ present in our bodies, diminishes over time as we age. At age 50, we only have about half as much in our bodies as we do at age 20. Low amounts of NAD+ are linked to several diseases from skin cancer to Alzheimer’s, cardiovascular disease, and multiple sclerosis. In theory, if we could chronically supplement ourselves with NAD+, we could see a slowing down or reversal of the age-related symptoms mentioned. However, NAD+ cannot diffuse through cell membranes. Thus, we can’t supplement it to ourselves through pills. One way we can circumvent this issue, is through the use of NAD+ precursors. Scientists noticed that more flexible substances could enter cells and turn into NAD+ inside. Ongoing research into the effectiveness of such precursors have just recently begun.

Another component to aging is the build of senescent cells. Over the course of our lives, our cells divides and copies its chromosomes. Each day, nearly 2 trillion cells divide. Because of how cell division works, they lose a small amount of DNA at the ends of their chromosomes. To protect themselves from this, additional long segments of DNA called telomeres are wrapped around the ends of the chromosomes.

After each cell division, the telomeres at the tips of the chromosomes become shorter and shorter. In some cells, this continues up to a point where the telomeres are entirely gone and they become senescent. CREDIT: ISTOCK AT https://www.istockphoto.com

In some cells, after a number of cell divisions, the telomeres will be entirely gone and the cells become senescent. Senescent cells accumulate in your body. Unlike normal cells that undergo programmed cell death (apoptosis) when they are damaged, senescent cells don’t. This becomes a problem as senescent cells harm tissue around them and are linked to many diseases that are age-related like diabetes and kidney failure.

Lastly, there’s stem cells. Stem cells are present throughout the body and remain in a non-specific state until they’re needed (e.g. for tissue repair). Unfortunately, the levels of available stem cells our bodies decline as we age, ultimately leading to our own decline as well. Without stem cells to renew tissue and help the body maintain its proper functionality, we become increasingly worn out, unable to replenish ourselves.

Stem cell illustration. CREDIT: ISTOCK available at https://www.istockphoto.com

The decline of NAD+ and stem cells, as well as the build-up of senescent cells harming the cells around them, are what we know of today to be the main components causing us to age and become old. In the following posts, I will go into more detail on each component and how they can be engineered and manipulated to help us fight aging and its devastating consequences. Aging is a devastating disease, diminishing your quality of life and causing a significant burden to your loved ones and to the society. There is a rising issue of there being more people of old age than there are people being born. This forces us to spend hundreds of millions of pounds on care for people who are unable to work and unable contribute to society, putting a massive strain on the global economy. If you’ve ever experienced a loved one on the verge of loosing their hearing, their vision and their minds — unable to take care of themselves — you might agree with the sentiment that no one deserves to be old.

Sources in appearing order:
Krafts, K. (2010). Tissue repair. Organogenesis, 6(4), pp.225-233.

Srivastava, S. (2016). Emerging therapeutic roles for NAD+ metabolism in mitochondrial and age-related disorders. Clinical snd Translational Medicine, 5(1).

Schultz, M. and Sinclair, D. (2016). Why NAD+ declines during aging: It’s destroyed. Cell Metabolism, 23(6), pp.965-966.

Johnson, S. and Imai, S. (2018). NAD+ biosynthesis, aging, and disease. F1000Research, 7, p.132.

van Roermund, C., Elgersma, Y., Sing, N., Wanders, R. and Tabak, H. (1995). The membrane of peroxisomes in Saccharomyces cerevisiae is impermeable to NAD(H) and acetyl-CoA under in vivo conditions. The EMBO Journal, 14(4), pp.3480-3486.

En.wikipedia.org. (2019). Precursors (chemistry). [online] Available at: https://en.wikipedia.org/wiki/Precursor_(chemistry) [Accessed 11 Oct. 2019].

Ratajczak, J., Joffraud, M., Trammell, S., Ras, R., Canela, N., Boutant, M., Kulkarni, S., Rodrigues, M., Migaud, M., Auwerx, J., Yanes, O., Brenner, C. and Cantó, C. (2016). NRK1 controls nicotinamide mononucleotide and nicotinamide riboside in mammalian cells. Nature Communications, 7(1).

Wu, L. and Sinclair, D. (2019). The elusive NMN transporter is found. Nature Metabloism, 1(1), pp. 8-9.

Bolden, J. and Lowe, S. (2019). [online] Sciencedirect.com. Available at: https://www.sciencedirect.com/sdfe/pdf/download/eid/3-s2.0-B9781455740666000159/first-page-pdf [Accessed 11Oct. 2019].

Chintamani (2017). Tricking a Cancer Cell into Committing Suicide or Apoptosis. Indian Journal of Surgery, 79(1), pp. 4-5.

Campisi, J. (2013). Aging, Cellular Senescence, and Cancer. Annual Review of Physiology, 75(1), pp. 685-705.

Brazier, Y. and Murrell, D. (2019). Stem cells: Sources, types, and uses. [online] Medical News Today. Available at: https://www.medicalnewstoday.com/articles/323343.php [Accessed 11 Oct. 2019].

Ahmed, A., Sheng, M., Wasnik, S., Bayling, D. and Lau, K. (2017). Effect of aging on stem cells. World Journal of Experimental Medicine, 7(1), p.1.

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