Genetics of Ageing

Ageing is an outcome of the pleiotropic effects of genes that specify other processes. The first pathway shown to influence ageing in animals was the insulin/ IGF-1 pathway. For several years, the molecular biologists who deal with the regulatory mechanisms did not seem to be interested to study ageing. But now we see that the process of ageing is subject to regulation by classical signalling pathways and numerous transcription factors. The discovery of these pathways was first done in short-lived organisms such as yeast and flies. There were many discoveries done to bring about the drugs which could slow down the process of ageing. Researchers say that mutations which slow down the process of ageing also lead to delay of age-related diseases.

One of the significant theories in ageing genetics is the DNA damage theory of Ageing. It explains that the consequence of an undamaged accumulation of naturally occurring DNA damages is termed as ageing. Here, damage means a slight alteration in the DNA having an abnormal structure. Both mitochondrial, as well as nuclear DNA damage, contribute to ageing, the main target here is the nuclear DNA damage as it contributes directly by increasing the cell dysfunction or indirectly by apoptosis (cell death).

Werner Syndrome (adult progeria) is a rare autosomal recessive disorder which is considered as the appearance of premature ageing. The changes found in the Gene transcription of Werner Syndrome are analogous to the Genes observed in normal ageing.