From our everyday movement to the complexity of our imagination and thoughts, human life is grounded in the bodies’ biology. However this one constant in our lives is subject to a limitation, this limitation is time. We are born, then grow until we reach our physical peak, at which point things start to deteriorate. The brain loses its plasticity, the body its mobility. But what if there was a way to prevent this? To slow it down, even. Here we come to a pioneering field of research known as biogerontology or, more colloquially, the study of ageing.

Throughout history much of biomedical research has been focused on treating acute conditions, infections and injuries. In the modern era where health outcomes are steadily improving (Ortiz-Ospina and Roser, 2016) the focus is shifting. Current models suggest that by the year 2100 projected global human lifespan will grow to anywhere between 80 and 100 (Gerland et al., 2022). Some gerontologists predict much higher means of 200+ (Richel, 2003). Whatever the exact number, we will not be getting any younger, at least without the threat of nuclear armageddon.

No one really dies of old age. Frailty takes hold, a breakdown of the body’s organic machinery. This is the current frontier in biomedicine: making the later years of life not just prolonged but also healthier. Already more research is being devoted to these areas. What might cause or accelerate ageing and how can it be dealt with?

One such study (Stoeger and Grant, 2022) suggests that ageing leads to DNA being damaged and RNA transcript lengths progressively shortening. This disrupts the coding for proteins and creates an imbalance between longer and shorter RNA transcripts. These shorter transcripts can often be linked to ageing factors such as increased inflammation. This study focuses on both the cause and prevention of ageing. In addition it tested several anti-aging methods that were evaluated and shown to have an effect on the RNA transcript lengths. These methods decreased the RNA length imbalance and resulted in potential enrichment to genes associated with longer lifespans in both mice and humans.

Such focus on the molecular is a key facet of the field. Looking into our most integral functions can help us understand not just what is going wrong and how to treat it but also what causes the process in the first place.

Focusing on a more holistic approach to treatments with an emphasis on homeostatic systems is integral to biogerontology, as exemplified by research in the field of senescent cells. Every time a cell divides in mitosis, DNA has to be copied. Each time this occurs DNA gets shorter. At a certain threshold of division these cells induce programmed self destruction. However this does not always work. The cells that remain are known as senescent cells. High levels of such are linked to both liver disease (Huda and liu, 2019) and obesity (Palmer and Gustafson, 2019). One study hoping to tackle this issue involved researchers genetically modifying mice to be more efficient at removing senescent cells. Importantly these mice lived thirty percent longer on average with improved kidney function and a reduced susceptibility to cancer (Callaway, 2016).

It is studies like these which demonstrate biological researchers’ ability to to change focus and anticipate for an increasingly ageing population. Through increased funding and research opportunities these areas will continue to expand, the pool of knowledge ever deepening. By thinking forward we may be able to improve the lives of future generations. A new way of being old emerging, allowing one to see beauty in ageing, as something to be welcomed.


Callaway, E. ‘Destroying worn-out cells makes mice live longer.’ Nature (2016).

Gerland, Patrick & Hertog, Sara & Wheldon, Mark & Kantorova, Vladimira & Gu, Danan & Gonnella, Giulia & Williams, Ivan & Zeifman, Lubov & Bay, Guiomar & Castanheira, Helena & Kamiya, Yumiko & Bassarsky, Lina & Gaigbe-Togbe, Victor & Spoorenberg, Thomas. World Population Prospects 2022: Summary of results. (2022).

Huda N, Liu G, Hong H, Yan S, Khambu B, Yin XM. ‘Hepatic senescence, the good and the bad.’ World J Gastroenterol. 2019 Sep 14;25(34):5069-5081. doi: 10.3748/wjg.v25.i34.5069. PMID: 31558857; PMCID: PMC6747293.

Ortiz-Ospina E. and Roser M. (2016). Global Health. Published online at Retrieved from: [Online Resource]

Palmer AK, Gustafson B, Kirkland JL, Smith U. ‘Cellular senescence: at the nexus between ageing and diabetes.’ Diabetologia. 2019 Oct;62(10):1835-1841. doi: 10.1007/s00125-019-4934-x. Epub 2019 Aug 27. PMID: 31451866; PMCID: PMC6731336.

Richel T. ‘Will human life expectancy quadruple in the next hundred years? Sixty gerontologists say public debate on life extension is necessary.’ J Anti Aging Med. 2003;6(4):309-14. doi: 10.1089/109454503323028902. PMID: 15142432.

Stoeger, T., Grant, R.A., McQuattie-Pimentel, A.C. et al. ‘Aging is associated with a systemic length-associated transcriptome imbalance.’ Nat Aging 2, 1191–1206 (2022).