The drug apparently mimics the effects on the body of the only known animal Planet.
Experts say the findings might indicate genes in humans that could be targeted to increase lifespan and possibly to identify additional genes important in ageing.
Dr. Linda Buck of the research center says it remains unclear why, depriving the body of all but the minimum amount of calories needed to survive seems to enhance longevity but the Seattle team believe they may have found an easier way to achieve the same effect.
Nematode worms are ideal subjects for studies into lifespan, they are similar in many ways to humans as they have a central nervous system and sexual reproduction; they also only live for only a matter of weeks.
Dr. Buck says they are unable to explain it but it is possible the drug disturbed the balance of two brain chemicals which help the nematode decide whether there is enough food around to justify laying eggs and this, might produce a “perceived, but not real” state of starvation.
The researchers say such life-extending benefits however come at a cost with weight gain and increased appetite some of the side effects which is why the drugs are not popular antidepressants.
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A team from the Trinity College Dublin and the Sanger Institute, Cambridge (UK), led by Dr Arpad Palfi and Dr Jane Farrar of the Smurfit Institute of Genetics, Trinity College Dublin used mutant mice that model the human eye disease retinitis pigmentosa (RP). The researchers compared these mice with wild-type mice, testing their hypothesis that changes in microRNA expression may be evident in retinal degeneration.
Retinitis pigmentosa is the most common form of inherited retinal degeneration affecting more than one million individuals worldwide. Progressive photoreceptor cell death eventually leads to blindness. Mutations in more than 40 genes have been linked to the disease and no therapy is currently available.
The team found very similar patterns of microRNA expression in retinas of two wild-type mouse strains, but, microarray profiling revealed that in these wildtype mice the patterns of microRNA expression differed between the brain and retina. Furthermore, there were clear differences in the microRNA expression patterns between wild type and mutant mice. The researchers found alterations greater than two-fold in the expression of 9 microRNAs in mutant mouse retinas compared with those of the wild-type mice. These microRNAs potentially regulate genes implicated in retinal diseases and genes encoding components involved in cell death and intracellular trafficking.
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