SIR2 and aging--the exception that proves the rule.
One of the holy grails of medicine is the possibility of an increase in lifespan without a decrease in vitality. However, the causes and processes of human aging are still unclear. One evolutionary theory is that in the post-reproductive stage of life, selective forces decline allowing many vital systems to deteriorate. This suggests that intervention will be difficult, if not impossible. However, molecular geneticists propose an aging process that is programmed (like other developmental processes) and regulated by single genes, meaning that intervention could be possible. Here, I discuss a way of reconciling these two views that could have major implications for healthcare.
Guarente
L
L
Dept of Biology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. leng@MIT.edu
D000375:Aging / Q000235:genetics* / Q000502:physiology*; D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics / Q000502:physiology; D005656:Fungal Proteins / Q000235:genetics / Q000378:metabolism; D006655:Histone Deacetylases / Q000235:genetics / Q000378:metabolism*; D006801:Humans; D008017:Life Expectancy; D008954:Models, Biological; D012441:Saccharomyces cerevisiae / Q000166:cytology / Q000235:genetics / Q000502:physiology; D038281:Silent Information Regulator Proteins, Saccharomyces cerevisiae; D056564:Sirtuin 1; D056565:Sirtuin 2; D037761:Sirtuins; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism*
D005656:Fungal Proteins; D038281:Silent Information Regulator Proteins, Saccharomyces cerevisiae; D015534:Trans-Activators; C087778:SIR2 protein, S cerevisiae; C447939:SIRT1 protein, human; D056564:Sirtuin 1; D056565:Sirtuin 2; D037761:Sirtuins; D006655:Histone Deacetylases