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Aging News & Information
Aging Discovery May Lead to Drug to Protect People
from Disease-Causing Genes
Einstein researchers say bad genes buffered by
longevity genes
Aug. 27, 2007 – Some day, maybe, you can take a
pill that mimics a special "longevity gene" and live to more than 100.
That's the vision of researchers who have found that people who do live
to be 100 have unique genes that protect them from the harmful effects
of bad genes that carry disease.
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People who live to 100 are known to have just as
many - and sometimes even more – of the harmful genes as younger people.
Then how did they live longer? Scientists at the Albert Einstein College
of Medicine of Yeshiva University say the secret behind this paradox is
just that the disease-carrying genes are prevented from doing their
destructive work by buffers created by longevity genes.
“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 Dr. Aviv Bergman, a professor in
the departments of pathology and neuroscience at Einstein and senior
author of the study, which appears in the August 31 issue of PLoS
Computational Biology.
To test this hypothesis, Dr. Bergman and his
colleagues examined individuals enrolled in Einstein’s Longevity Genes
Project, initiated in 1998 to investigate longevity genes in a selected
population: Ashkenazi (Eastern European) Jews.
They are descended from a founder group of just
30,000 or so people. So they are relatively genetically homogenous,
which simplifies the challenge of associating traits (in this case,
age-related diseases and longevity) with the genes that determine them.
Participating in the study were 305 Ashkenazi Jews
more than 95 years old and a control group of 408 unrelated Ashkenazi
Jews. Centenarians are so rare in human populations—only one in 10,000
people live to be 100—that “longevity” genes probably wouldn’t turn up
in a typical control group. Longevity runs in families, so 430 children
of centenarians were added to the control group to increase the number
of favorable genes.
All participants were grouped into cohorts
representing each decade of lifespan from the 50’s on up. Using DNA
samples, the researchers determined the prevalence in each cohort of 66
genetic markers present in 36 genes associated with aging.
As expected, some disease-related gene variants
were as prevalent, or even more prevalent, in the oldest cohorts of
Ashkenazi Jews than in the younger ones.
And 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,” says Dr. Bergman.
The Einstein researchers were able to construct a
network of gene interactions that contributes to the understanding of
longevity. In particular, they found that the favorable variant of the
gene CETP acts to buffer the harmful effects of the disease-causing gene
Lp(a).
If future research finds that a single longevity
gene buffers against several disease-causing genes, then drugs that
mimic the action of the longevity gene could help 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.”
Meanwhile, the Einstein researchers are greatly
expanding their longevity research: From the 66 genetic markers examined
in this study, they are now using a high-throughput technology that
allows them to assay one million genetic markers throughout the human
genome. The goal is to find additional genetic networks that are
involved in the process of aging.
Other Einstein researchers involved in the study
were Gil Atzmon, Kenny Ye, Thomas McCarthy and Nir Barzilai.
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