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CHAPTER 1 A biological perspective of ageing
Florent Guerville1,2 and Maël Lemoine2
1 Clinical Gerontology Department, Bordeaux University Hospital, Bordeaux, France
2 ImmunoConcept Lab, CNRS UMR5164, University of Bordeaux, Bordeaux, France
Introduction
Ageing is not a technical word introduced recently into biology to refer to a well‐circumscribed, specific phenomenon. It comes from common language. In the last century, biologists tried to give the word a precise biological translation. Yet it still has a vague biological meaning, despite all the progress accomplished in discovering the mechanisms of ageing. Indeed, so‐called ‘mechanisms of ageing’ are generally mechanisms involved in the average acceleration or retardation of death in a population or the manifestation of signs usually attached to ageing. This is the best proxy we have, but the results should always be viewed with care. On the one hand, manipulating certain mechanisms (e.g. of metabolism) may advance or retard the average age of death without those mechanisms being necessarily involved in ‘ageing’ in the first place. On the other hand, some syndromes or diseases, like progeria, may mimic ageing without much of a link between the pathological process at hand and physiological, normal ageing. Such are the consequences of having to use a vague word in biology. However, the importance of this process to the understanding of human health is such that this concept cannot just be abandoned. This chapter offers an overview of our biological knowledge of ageing.
There are two complementary approaches to the biology of ageing. In the populational approach, the focus is on the properties of ageing populations, some of which can be extrapolated to individuals. In the physiological approach, one investigates the mechanisms of ageing at the level of organisms, organs, tissues, cells, or even molecules.
A populational perspective on ageing
Incidence of death is the proportion of individuals of a population who die within a period of time. In the human population, as well as other populations, it is known to increase exponentially from the age of maturity to maximum lifespan (see Figure 1.1). Such curves are called Gompertz models. They have been known and studied since the nineteenth century.1 Were the curve to depend only on extrinsic factors of death like accidents, predation, starvation, or war, it would not show any regular, time‐dependent pattern (a recent example is the naked mole‐rat,2 as shown in Figure 1.2). In contrast, the typical shape of the curve is commonly interpreted as an effect of intrinsic factors of death. These chiefly consist of diseases. They are both more frequent and deadlier with time because they are somehow catalysed by ageing. Ageing is, therefore, the primary intrinsic factor of death. It has also become the leading cause of death in most human populations and populations of domestic animals, well before infectious diseases, accidents, and starvation.
Focusing on the right‐hand part of the curve and what happens at the end of life, three facts must be emphasised. The first is that after the age of 80, the incidence of death still increases, but more slowly – and it continues to slow with time. The incidence of death even seems to reach a maximum. This so‐called ‘late‐life mortality plateau’, i.e. the time of life when the incidence of death ceases to increase and becomes constant, has been documented for Melanogaster 3 and in several other species, but not for mammals. For humans, it remains a matter of debate. The discussion revolves around the small number of people reaching extreme old age and the reliability of the data.4 If the human population reached a late‐life mortality plateau, the incidence of death would stabilise around .5 after age 105–110. In other words, so‐called ‘supercentenarians’ would have a 1 in 2 chance of dying before the end of the year, whether they were 110 or 122 (age of Jeanne Calment at death). More importantly, the process of ageing seems to slow and perhaps even stop at some point. If this process does stop, then there is no intrinsic maximum lifespan for the human species. Hazard alone must then explain why the very few people reaching extreme old age are exceedingly unlikely
