Ageing is thought to be our inevitable fate – an accumulation of wisdom, as well as mutations that reside in our DNA with the passage of time. In biogerontological terms (the study of ageing), it is described as ‘senescence’, which encompasses the molecular, cellular, and physiological deteriorations that together drive a heightened risk of disease and mortality (Rodríguez et al., 2017). Although we arrive at old age in better health than ever before in human history, Alzheimer’s, rheumatism, cancer, and other prevalent age-related diseases, are still the leading causes of death today. But what if ageing were targeted as the overriding disease itself? Would that make us prepared to cure ageing? What is ageing really? While most of us are aware of the physical changes that arise as we age, such as body aches, slower recovery, or worse sleep, we are less aware of the changes that occur at a cellular level. The wearing of our telomeres is one of the most renowned molecular effects of senescence. Telomeres are caps on the ends of our chromosomes that protect our DNA from erosion. As we age and accumulate cell divisions, our telomeres slowly shrink in size, eventually reaching what scientists call ‘Hayflick’s limit’. Like an innate molecular clock, once our telomeres reach their Hayflick’s limit, the cell can either become cancerous (dividing uncontrollably) or senescent, entering the slow trajectory into old age (Aviv and Shay, 2018). Many competing theories of ageing exist. One that could explain some of the abnormal accumulation of various compounds as we age is Blagosklonny’s ‘hyperfunction’ theory of ageing (Blagoskonny, 2006). It hypothesises that our bodies continue producing certain compounds beneficial in early life, which accumulate as we age, like a tap left on. This idea could explain abnormal accumulation processes such as the build-up of amyloid-beta observed in Alzheimer’s disease – an age-related neurodegenerative disease. How does ageing affect our brain? Not even our body’s immune system, a well-orchestrated process that we rely on to protect us from infections, is ‘immune’ to ageing. The decline in our protective responses experienced with ageing is termed ‘immunosenescence’ (Aiello et al., 2019). It is why infections that we could have easily beaten as children take much longer to clear in the elderly. The brain is one vital organ affected by the ageing immune system. For decades, the brain was considered an immune-privileged environment, but this has been overturned in the past few years. Immune cells have been found to play an important role in maintaining the brain’s ecosystem. When immune cells (such as microglia in the brain) become sluggish, they are less capable of switching off inflammation induced by an immune response. This chronic low-grade inflammation in the central nervous system (CNS), or ‘neuroinflammaging’ exacerbates neurodegeneration (Costantini et al., 2018). Age-related changes are not limited to immune cells in the CNS but can also have an impact on the blood-brain barrier (BBB), a crucial immunological feature of the CNS, that regulates the movement of biological substances between the blood and the brain. Studies have highlighted phenotypic and mechanistic changes in the BBB, that disrupt its signalling and function, and can result in the leakage of harmful immune cells and proteins into the brain (Erickson & Banks, 2019). As a result, the ageing immune system is associated with a decline in cognitive functioning and memory and is characteristic of neurodegenerative disorders like Alzheimer’s and Parkinson’s disease. Not only do key immune cells such as microglia or astrocytes forego their protective roles in such disorders, but they also start promoting inflammation and secrete a whole host of toxic compounds such as ‘cytokines’ (Shao, Gearing and Mirra, 1997; Wang et al., 2015). Could ageing be a disease? And what if it is? Not all species experience ageing. Lobsters and tortoises, for example, display no signs of ageing (Congdon et al., 2001). If ageing isn’t universal or natural, then could it be a wide-spread disease? We think it could be. According to the Merriam-Webster dictionary, a disease is any condition that “impairs normal functioning and is typically manifested by distinguishing signs and symptoms”, criteria that align with changes observed in ageing. If ageing is a disease, then surely we have a moral obligation to cure it? And would it not be more effective to cure ageing holistically, as opposed to tackling each age-related disease individually? You may be concerned with overpopulation, but the same can be said for curing any other disease. For example, we don’t perceive curing infant mortality to be unethical because it can exacerbate overpopulation. In the past century alone, we have practically doubled our life expectancy from around 47 years of age to close to 80 in the US (Centers for Disease Control and Prevention/National Center for Health Statistics [CDC/NCHS], 2012, 2013). Why is this any different? But as we push the limits of our ‘healthspan’ further (a term used to describe the healthy period of one’s life), it will be important for society to ensure that the right policies are in place to regulate and democratise the cure to ageing. What do you think? For a fun and informative podcast on ‘rapamycin’, a drug which has been touted to slow down some pathological processes exacerbated by ageing, listen to this podcast. By Alexandra Petrache, Dana Al-Juburi and Sidak Seth References: Akintola AA, van Heemst D. Insulin, aging, and the brain: mechanisms and implications. Front Endocrinol (Lausanne). 2015 Feb 6;6:13. doi: 10.3389/fendo.2015.00013. PMID: 25705204; PMCID: PMC4319489. Aiello, A. et al. (2019) “Immunosenescence and its hallmarks: How to oppose aging strategically? A review of potential options for therapeutic intervention,” Frontiers in Immunology, 10. Available at: https://doi.org/10.3389/fimmu.2019.02247. Aviv, A. and Shay, J.W., 2018. Reflections on telomere dynamics and ageing-related diseases in humans. Philosophical Transactions of the Royal Society B: Biological Sciences, 373(1741), p.20160436. Blagosklonny MV. Aging and immortality: quasi-programmed senescence and its pharmacologic inhibition. Cell Cycle. 2006 Sep;5(18):2087-102. doi: 10.4161/cc.5.18.3288. Epub 2006 Sep 15. PMID: 17012837. Centers for Disease Control and Prevention/National Center for Health Statistics [CDC/NCHS], 2012, 2013 Congdon, J.D., Nagle, R.D., Kinney, O.M. and van Loben Sels, R.C., 2001. 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