[DIYbio] Re: Prospects of anti-aging research

Relevant summary article; open access.

http://rstb.royalsocietypublishing.org/content/365/1537/147.full

The new biology of ageing

Linda Partridge*

Institute of Healthy Ageing and GEE, UCL, Darwin Building, Gower Street, London WC1E 6BT, UK  l.partridge@ucl.ac.uk

doi: 10.1098/rstb.2009.0222 Phil. Trans. R. Soc. B 12 January 2010 vol. 365 no. 1537 147-154

Excerpt ( I suggest  reading the entire article ):

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Perhaps the single most important advance in ageing research in recent years has been discovery of mutations in single genes that extend the lifespan of laboratory animals. They first came to light as a result of a systematic chemical mutagenesis screen for lifespan-extending mutations in C. elegans (Klass 1983). Subsequent work with these mutations (Friedman & Johnson 1988), and further screening (Kenyon et al. 1993), revealed that it was possible to double the lifespan of the worm with a mutation in a single gene. Furthermore, rather than solely prolonging the moribund period at the end of the life, the mutations caused the worms to remain healthy and youthful for longer (Kenyon et al. 1993). The mutated genes were discovered to encode components of an invertebrate insulin/insulin-like growth-factor-like signalling (IIS) pathway (Kimura et al. 1997; Lin et al. 1997; Ogg et al. 1997). These findings came as a considerable surprise, because a signalling pathway previously associated with control of growth and metabolism in mammals now turned out to play a role in determination of lifespan in a distantly related invertebrate.

Mutations with similar effects on lifespan were soon discovered in other model organisms. For instance, a similar screening effort in yeast led to the discovery that over-expression of a protein deacetylase, SIR2, extended replicative lifespan (Sinclair & Guarente 1997; Kaeberlein et al. 1999), while mutations in methuselah in Drosophila increased fly lifespan (Lin Seroude & Benzer 1998). Likewise, in the mouse, mutations in genes encoding transcription factors involved in the development of the pituitary gland resulted in long-lived dwarf mice (Brown-Borg et al. 1996). By the late 1990s, it was firmly established that lifespan of these model organisms could indeed be extended by mutations in single genes.

It had also been known since the 1930s that an environmental intervention, dietary restriction (DR), could produce substantial increases in lifespan in laboratory rodents (McCay et al. 1935). Although the exact mechanisms at work still await full elucidation, detailed study of DR rodents has demonstrated a broad-spectrum improvement in health and a delay in or amelioration of the impact of a wide range of ageing-related diseases (Masoro 2005, 2006). For instance, the animals are protected against cancer, cataract, diabetes, motor decline, osteoporosis and nephropathy (Weindruch & Walford 1988). These findings suggested that, in principle, multiple aspects of the ageing phenotype could be simultaneously ameliorated by a single intervention, albeit, in the case of DR, a complex one.

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## Jonathan Cline

## jcline@ieee.org

## Mobile: +1-805-617-0223

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