One of the earliest blog posts I wrote was about ageing. However, it was too convoluted and meandering even by my standards, so I set it to private, pending a rewrite. But I occasionally get questions about ageing, so I might as well do a quick summary.
There are two major hypotheses about ageing: antagonistic pleiotropy and mutation accumulation, first suggested by Medawar (1952).
The antagonistic pleiotropy hypothesis was properly treated and polished by Williams (1957) and Hamilton (1966). It’s a theoretically sound idea, but with little emprical evidence. It basically states that there are alleles/gene loci that affect fitness differentially depending on the age of the individual. The ones that have a positive effect at a young age and deleterious effect at older ages will be kept because most animals reproduce when they are younger, i.e. at the time of reproduction, the deleterious effects would not have manifested yet. The lack of empirical support is not really such a strong point against it, as it would take quite a bit of luck to identify such a locus in wild populations.
The mutation accumulation hypothesis has the same basis in having alleles with differential fitness at different ages, but does away with the selection bit. Basically, later in life, there is less selection acting on the genome, meaning that alleles with deleterious effects can accumulate without being weeded out, so the deleterious mutation accumulate (akin to genetic drift), bringing about the deleterious effects otherwise known as senescence.
Of course, it should be obvious that these aren’t mutually exclusive. And these two hypotheses are the genetic ones – there are also the typical hypotheses that attribute ageing to purely envirnomental causes (you can guess their gist intuitively). On a personal note, I will say that it seems rather dubious to me that such a multifaceted process as ageing could be chalked up to just genetic or just environmental causes. Of course, I could be wrong (this also is very, very far away from my field). I hate to jump on a bandwagon, but if I were in charge of starting up a research program for investigating ageing, I would first of all explicitly not use any laboratory animals – ageing is intricately tied to life history and fitness, so wild populations are the way to go (with the usual problem that there are way too many confounding factors) – and I would also place a very high emphasis on epigenetics to locate loci that are potentially involved.
As you can tell, I’m not a fan of simple research programs.
Hamilton WD. 1966. The moulding of senescence by natural selection. Journal of Theoretical Biology 12, 12-45.
Medawar PB. 1952. An Unsolved Problem in Biology.
Williams GC. 1957. Pleiotropy, natural selection, and the evolution of senescence. Evolution 11, 398-411.