Max Planck Research Group: Modeling the Evolution of Aging, Max Planck Institute for Demographic Research, Konrad Zuse Strasse 1, 18057, Rostock, Germany.
Biogerontology. 2013 Feb;14(1):99-105. doi: 10.1007/s10522-012-9410-7. Epub 2012 Nov 17.
Senescence evolved because selection pressure declines with age. However, to explain senescence it does not suffice to demonstrate that selection pressure declines. It is also necessary to postulate biological mechanisms that lead to a deteriorated state of the organism at high ages, but not before. This has lead to the invocation of 'age-specific' genes or processes, a concept which is prone to be interpreted too freely. Events do not happen after a certain amount of time has passed. They need initiation, which means that senescence is required to be a continuous process. As a result, a change at a particular age cannot arise in isolation from changes at other ages, in particular not in isolation from changes at the ages nearby. These mechanistic constraints are not without consequence for the patterns of mortality and fecundity that can evolve. I conclude that from purely logical considerations, senescence is characterized as continuous rather than age-specific deterioration. These considerations guide (theoretical) research in the direction of investigating how continuous somatic change arises, rather than focusing at age-specific events.
衰老是因为随着年龄的增长,选择压力下降而进化的。然而,仅仅证明选择压力下降并不能解释衰老。还需要假设导致生物体在高年龄时状态恶化的生物机制,但在这之前不会。这导致了“年龄特异性”基因或过程的假设,这个概念很容易被过度解读。事件不会在经过一定时间后发生。它们需要启动,这意味着衰老是一个连续的过程。因此,特定年龄的变化不能与其他年龄的变化孤立地发生,特别是不能与附近年龄的变化孤立地发生。这些机制上的限制对于可以进化的死亡率和生殖率模式没有影响。我得出的结论是,仅仅从逻辑上考虑,衰老是连续的,而不是特定年龄的恶化。这些考虑引导(理论)研究朝着调查连续的体细胞变化如何产生的方向发展,而不是关注特定年龄的事件。