In our opinion, what we refer to as ageing is not chronological, but biological in nature. The ageing process is made up of a collection of interwoven biological changes and a progressive loss of physiological integrity. This ultimately leads to dysfunctional changes throughout our cells, tissues and organs, increasing our vulnerability to disease and ultimately leading to death.
There is nothing in biology yet found that indicates the inevitability of death. This suggests to me that it is not at all inevitable […].-Richard Feynman, The Pleasure of Finding Things Out
Many argue that ageing itself should be viewed as a disease, or at least a collection of diseases, and that it can be treated as such. Others regard ageing as too complex and too diverse a problem to be considered a disease. Regardless of whether ageing is a disease or not, there is no reason to believe that ageing cannot be slowed or cured through science, but to do this, we must understand the fundamental changes that underlie the ageing process. As mentioned, ageing is a collection of interconnected problems, and is unlikely to be fully explained by any single factor. We refer to these ‘common denominators’ of ageing as the hallmarks of ageing.
In 2013 in the journal CELL, there appeared an article that posited the hallmarks of ageing and the role each played in the overall systemic dysfunction associated with the ageing process. The hallmarks include: genomic instability, telomere attrition, epigenetic alterations, loss of proteostasis, deregulated nutrient sensing, mitochondrial dysfunction, cellular senescence, stem cell exhaustion, and altered intercellular communication. Don’t worry if you don’t know what any of these terms mean, as this series of articles will explore each of them in turn, how they are affected by ageing and how we may be able to fix them.
A major challenge is to dissect the interconnectedness between and among the candidate hallmarks and their relative contributions to aging, with the final goal of identifying…targets to improve human health during (chronological) aging, with minimal side effects.The Hallmarks of Aging
Thus, by breaking ageing down into its constituent components, we may study which ones contribute the most to the ageing process as a whole, and we may begin to search for links between all these hallmarks that may lead us to targets for reversing the ageing process entirely. This is no easy task due to the the incredible complexity of these processes. Such missing links would be likely to lie at the most basic levels of physiological or biochemical activity, and it would need to be shown that modulating them could ameliorate or worsen related hallmarks of ageing.
We consider the processes mentioned above to be the hallmarks of ageing because they are the common denominators of ageing not only amongst humans, but also throughout different species. Furthermore, at least one or two of them (and in many cases, most of them) are found in all chronic diseases of ageing. Finally, the study of genetic mutations affecting these hallmarks, both in animals and humans, suggests that causal relationships exist between them and the ageing process.
Over the following series of articles, we will discuss each hallmark of ageing in more detail, including what exactly they are, how they change during ageing, and how we might be able reverse them in the future. Hopefully, by the end of this series, you will have a wider understanding of what actually makes us age.
What Is Genomic Instability? – The Hallmarks Of Ageing Series
What Is Telomere Attrition? – The Hallmarks Of Ageing Series
What Are Epigenetic Alterations? – The Hallmarks Of Ageing Series
What Is Deregulated Nutrient Sensing? – The Hallmarks Of Ageing Series
What Is Mitochondrial Dysfunction? – The Hallmarks Of Ageing Series
What Is Cellular Senescence? – The Hallmarks Of Ageing Series
What Is Stem Cell Exhaustion? – The Hallmarks Of Ageing Series
What Is Altered Intercellular Communication? – The Hallmarks Of Ageing Series
The Hallmarks of Aging: https://dx.doi.org/10.1016%2Fj.cell.2013.05.039
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