New-found gene could play role in aging from birth
- July 22, 2014
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It's something of an eternal question: Can we slow or even reverse aging? Although genetic manipulations can alter some cellular processes, not so much is known about the mechanisms of the aging process in living things.
Now scientists have found in animal models that one gene plays a surprising role in aging that can be detected early on in development. They say the discovery could point toward the possibility of one day using therapeutics, even some commonly used ones, to manipulate the aging process itself.
This “developmental gene, known as Spns1, may mediate the aging process,” said Shuji Kishi, a professor at the from the Florida campus of The Scripps Research Institute who led the study, published by the journal PLoS Genetics. “Even a partial loss of Spns1 function can speed aging.”
Using various genetic approaches to disturb Spns1 during the embryonic and/or larval stages of zebrafish-which have emerged as useful for studying diseases associated with development and aging-the scientists said they produced some models with a shortened life span, others that lived long lives.
While most studies of “senescence”-decreases in a cell's power of division and growth-have focused on later stages of life, the new study explores early stages. “Mutations to Spns1 both disturbs developmental senescence and badly affects the long-term bio-chronological aging process,” Kishi said.
The study found that Spns1, along with a pair of “tumor suppressor genes,” called beclin 1 and p53, can influence senescence through two different mechanisms: the Spns1 defect was enhanced by Beclin 1 but suppressed by ‘basal' p53. Spns1 also was found to hinder autophagy, a process whereby cells remove unwanted or destructive proteins and balance energy needs during various life stages.
Building on their insights from the study, Kishi and his colleagues noted in the future therapeutics might be able influence aging through Spns1. He said a commonly used antacid, Prilosec, has been shown to temporarily suppress autophagic abnormality and senescence seen in the Spns1 deficiency.
Source : world-science.net