It is estimated that by 2050, 1 in 5 people will be over 60 years old. Expectations of the ageing society pose a major challenge to doctors and biologists worldwide. But is there hope? Can we ameliorate diseases of old age? Can we cure ageing?
To answer this, we must firstly focus on what causes ageing. From the pool of countless mechanistic theories of ageing, two major models emerge. The first theory coined by D.Harman is arguably the most popular explanation of ageing on the molecular level. It states that reactive oxygen species (free radicals), which are formed inside the cells during various metabolic processes, lead to decline in function of cell constituents such as proteins, DNA and lipids, causing ageing.
An opposing theory was proposed by M. Blagosklonny, who says that ageing is not a decline in function, but a hyperfunction. To put it simply, developmental programmes, which evolved to maximise one’s wellbeing and chances of reproduction, can metaphorically turn to the dark side of the force after development has completed, causing ageing. He uses a bathtub analogy in which developmental processes are designed to fill the bathtub. However, there is no one to turn the faucet off, so eventually the programme designed to fill the bathtub will cause flooding in the bathroom (ageing).
Ageing can be defined as a set of pathologies, some of which could lead to age-related mortality. For instance, skin wrinkling, although undesired, will never lead to one’s death. On the other hand, cardiovascular disease, which is highly associated with ageing, can kill you in a blink of an eye. It is important to recognize that no one has ever died of old age, but many people have died as a result of agerelated pathologies. One of the ideas that have recently emerged from research into old age is that in order to understand the causes of ageing, we must firstly document and investigate all of the age-related pathologies. Only with that knowledge we can begin to untangle complicated mysteries of why do we age and how to cure ageing.
Experimenting on humans is not only unethical and illegal. It also takes a long time. Humans live for about 80 years, so even if we want to create “a longlived” human mutant (we all love those X-men movies), or to see the results of ameliorating a pathology within the length of life, we will have to wait for at least 80 years to see the experimental results. No one has capacity for such a length of time (or amount of funding).
This is why scientists use simple, shortlived organisms as models to test their theories. The favourite model organism of ageing research is Caenorhabditis elegans worm – a small, transparent nematode that can be easily housed and cultivated in large numbers. They live for about 3 weeks and the most fascinating thing about them is that even if you have never seen a C. elegans worm before in your life, you can tell if the worm is old. Their outer cuticle wrinkle, they barely move, don’t feed and generally look as miserable as a worm can look.
Biologists in this field hope that if we understand why these tiny worms age, it might open up the doors to understanding human ageing. Of course, by looking at worms, we are not interested in them per se. We are interested in the common ancestor of worms and humans. Regardless of millions of years of evolution, mechanisms present in that common ancestor possibly are still present in our bodies today.
About the author:
Kalina Cetnar has just finished her Masters in Human Genetics at UCL. During her final year project she investigated lipotoxicity in C.elegans. She is mostly interested in bridging science and industry and increasing public understanding of science.