Six conditions cause the majority of deaths in the world, these include dementia and cardiovascular disease. Traditionally, we’ve looked at these conditions through the lens of what goes wrong individually, such as blocked arteries around the heart or tangles of proteins that impair electrical signalling in the brain. But the common denominator is actually ageing.

As grandiose and esoteric as that sounds, ageing and the processes that govern ageing are what we need to be tackling if we want to better manage or even prevent these conditions of older age.

And with me to discuss why and how we age is Richard Faragher. He’s Professor of Biological Gerontology at the University of Brighton, and has dedicated his career to understanding the ageing process and what we can do to improve this inevitable phase of life.

As you can tell from today's episode, Richard is a passionate advocate for older people and can wax lyrical about the history of the gerontology field.

A few definitions before we dive into the episode I think will be helpful for people who are new to the research.

There are agreed “hallmarks” of ageing that are a description of processes, such as metabolism and DNA repair functions, that go awry as we grow older. Ageing is caused by these changes at the molecular level that lead to downstream effects like disease and degeneration.

Cell senescence is what happens at the end of a cell's lifespan, where they become dysfunctional and need to be removed by immune cells. However in older age, it can become more troublesome for your immune system to clear away these senescent cells and increasing inflammation ensues.

Senolytics are compounds or drugs that have been designed to selectively eliminate these senescent cells. And the hope is that they can mitigate a range of age-associated conditions like arthritis, cataracts, dementia and more.

Trigger warning. We discuss a graphic analogy for senescent cells using suicide, so I just wanted to give a heads up for anyone who might find that analogy uncomfortable.

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