Saturday 25 October, 2014

“Longevity” gene behind living beyond 100 uncovered

Published On: Sat, Aug 25th, 2007 | Bioinformatics | By BioNews

Aug. 25 : Scientists at the Albert Einstein College of Medicine of Yeshiva University have found out why some people live to 100 or more, despite the fact that they have as many, or sometimes even more, harmful gene variants as younger people.

The scientists have uncovered favourable “longevity” genes that provide very old people with protection against the harmful effects of bad genes.

Reported in the journal PLoS Computational Biology, the novel approach used by the researchers may lead to the development of new drugs to protect against age-related diseases.

“We hypothesized that people living to 100 and beyond must be buffered by genes that interact with disease-causing genes to negate their effects,” says senior study author Dr. Aviv Bergman, a professor in the departments of pathology and neuroscience at Einstein.

In order to test their hypothesis, the researchers examined individuals enrolled in Einstein’s Longevity Genes Project, initiated in 1998 to investigate longevity genes in a selected population, viz, Ashkenazi (Eastern European) Jews.

Since Ashkenazi Jews are descended from a founder group of about 30,000 people, they are relatively genetically homogenous. This simplifies the challenge of associating traits-such as age related diseases and longevity-with the genes that determine them.

In all, 305 Ashkenazi Jews more than 95 years old and a control group of 408 unrelated Ashkenazi Jews participated in the study. They were grouped into cohorts representing each decade of lifespan from the 50′s on up.

The researchers tested DNA samples collected from each cohort, and determined the prevalence of 66 genetic markers present in 36 genes associated with ageing. Some disease-related gene variants were as prevalent or even more prevalent in the oldest cohorts of Ashkenazi Jews than in the younger ones.

As Dr. Bergman had predicted, genes associated with longevity also became more common in each succeeding cohort.

“These results indicate that the frequency of deleterious genotypes may increase among people who live to extremely old ages because their protective genes allow these disease-related genes to accumulate,” he says.

The researchers also constructed a network of gene interactions, which enabled them to find that the favourable variant of the gene CETP acts to buffer the harmful effects of the disease-causing gene Lp(a).

If future research also shows that a single longevity gene buffers against several disease-causing genes, the finding may lead to drugs that mimic the action of the longevity gene to protect against cardiovascular disease and other age-related diseases.

“This study shows that our approach, which was inspired by a theoretical model, can reveal underlying mechanisms that explain seemingly paradoxical observations in a complex trait such as aging,” says Dr. Bergman.

“So we’re hopeful that this method could also help uncover the mechanisms-the gene interactions-responsible for other complex biological traits such as cancer and diabetes,” he added.

Meanwhile, from the 66 genetic markers examined in this study, the researchers are now using a high-throughput technology that allows them to assay one million genetic markers throughout the human genome. Their goal is to find additional genetic networks that are involved in the process of ageing. (ANI)

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