The recent announcement of a new approach to selective forcing self-destruction via apoptosis in senescent cells, and the prospects of using it as a therapy to reverse the accumulation of such cells and their contribution to aging, produced a wave of attention from the mainstream media. As is usually the case, little of that attention was well-informed or particularly discriminating when it came to the large differences in expectation value for potential ways to intervene in the aging process. When it comes to impact on age and age-related disease, clearing senescent cells is in a completely different category from, say, calorie restriction and calorie restriction mimetic drugs, but you wouldn't know that if your only source of information is the press.

Aging is caused by accumulated molecular damage of various sorts, damage that occurs as a side-effect of the normal operation of cellular biochemistry. That damage then causes secondary and later forms of damage and dysfunction, a growing chain of cause and consequence that ends with age-related diseases and death. Broadly speaking, there are two approaches to aging as a medical condition. The first, and by far the most common approach is to tinker with the operation of metabolism in order to modestly slow down the accumulation of damage - such as via replicating the calorie restriction response shown to lengthen life in short-lived species. This typically involves drug discovery and mapping cellular biochemistry in search of points at which to intervene, the latter of which is an enormously expensive and slow process. The research community doesn't have anywhere near the level of understanding needed to proceed rapidly in this effort, and this is well illustrated by the past two decades spent in search of ways to safely mimic the calorie restriction response. There is very little of practical use to show for that yet, despite the enormous outlay in time and funding.

The second approach is to repair the molecular damage that is the root cause of aging. Unlike the full extent of cellular biochemistry in metabolism and aging, that damage is well cataloged and well understood - what isn't known are the full details of how it interacts to cause specific manifestations of aging. That knowledge isn't needed in order to produce meaningful outcomes, however. To the extent that funding can be found, the work of repairing this damage could move ahead rapidly. Unfortunately, outside a few areas such as amyloid clearance in Alzheimer's disease and some portions of the stem cell field, this isn't a majority concern in the research community. Even senescent cell clearance, now a very exciting area with a great deal of venture funding for commercial development, was a poorly funded backwater as recently as six years ago. Unfortunately, that is presently the position for other equally important areas of repair, such as clearance of cross-links that damage elasticity in blood vessels and other tissues. There remains a great deal of work to do in order to give repair of the causes of aging the prominence it merits.

The search to extend lifespan is gaining ground, but can we truly reverse the biology of ageing?

It was once a fringe topic for scientists and a pseudo-religious dream for others. But research into the biology of ageing, and consequently extending the lifespan of humans and animals, has become a serious endeavour. The true promise of ageing research is that rather than tackling individual diseases one at a time, a single drug would treat all the diseases that arise in old age, at once. The idea of extending human life makes some uneasy, as preventing death seems unnatural. But this is already happening. Drugs and interventions developed over the past century that have almost doubled human life expectancy could be considered as anti-ageing. But when we talk about an anti-ageing pill, we mean one that targets the process of ageing itself. There is already a list of such drugs shown to extend the lives of lab animals. Many of these work through mimicking the effects of a near starvation diet. Calorie restriction has for over 80 years been the most well-studied intervention known to delay ageing. The willpower required to maintain a near starvation diet for an entire lifetime is beyond most. But regular, short term calorie restriction has strong benefits for metabolic health. Animal studies show a reliable extension in lifespan during intermittent fasting. Early on, the effectiveness of restricting calories led scientists to hunt for genes that mediated these effects, but the long-term effects of restricting calories on ageing in humans have yet to be fully characterised, and such a study in humans would be difficult to perform. Another anti-ageing strategy is one called "senolysis": that is, killing off old and damaged or "senescent" cells. These cells take up space, grow larger, and release substances that cause inflammation. When mice are genetically engineered so that it is possible to kill off senescent cells, health is drastically improved and animals live 20 to 30% longer. The hunt is now on for "senolytic" drugs, which can selectively kill off senescent cells. One company, UNITY Biotechnology, recently raised US$116 million to achieve this.

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