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bioquest
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Could somebody, possibly, provide a list of the mutations that cause aging- the specific mutations- "hotspots" and/or discuss that with me (ie you could pm me) thanks
NIH Awards Einstein Researcher $11.2 Million to Study Genome Instability as a Cause of Aging
August 27, 2009— (BRONX, NY) — The National Institutes of Health (NIH) has awarded Albert Einstein College of Medicine of Yeshiva University a five-year, $11.2 million grant to study the impact of damage to DNA on aging and disease. Research funded by this grant, and conducted by a consortium of scientists, could reveal the role of genome maintenance systems in delaying aging and will begin to explore novel interventions to maintain health in old age.
Led by Jan Vijg, Ph.D., chairman of genetics at Einstein, the research project will build on the consortium's previous, internationally recognized work involving mice that undergo accelerated aging. This research has shown that interfering with the cellular processes responsible for DNA repair leads to what appears to be premature aging in these animals. These results indicate that accumulating DNA errors may underpin the aging process.
The investigators in the consortium now plan to see if treatments based on these results can extend life spans of mice bred to have short lives. "We can try to use interventions that are based on alleviating DNA damage," Dr. Vijg says. "One approach, for example, could be the use of antioxidants, which neutralize free radicals, the chemicals that contribute to DNA damage."
Altogether, the research project involves four main areas of study:
■unraveling the mechanisms that lead from DNA damage to premature as well as normal aging
■testing the role of DNA maintenance and repair as a pro-longevity system in humans
■developing sets of blood-based biomarkers that indicate premature aging in mouse models, and validate these biomarkers in normally aging mice and in humans
■developing new, experimental interventions that neutralize symptoms of premature aging in the short-lived mice
The NIH program project grant has funded five groups of scientists who are working on interrelated parts of the project's four research areas. In addition to Dr. Vijg's group, another Einstein team is headed by Yousin Suh, Ph.D., associate professor of medicine, and of genetics. Yousin Suh, Ph.D.Dr. Suh will take advantage of a unique Einstein resource: tissue samples from Ashkenazi Jewish centenarians — living to age 100 and beyond. Using this relatively homogeneous population, brought together by her Einstein collaborator, Nir Barzilai, M.D., Dr. Suh will look for gene variations that are associated with longevity. Her team will test these
"longevity genes" by inserting them into otherwise ordinary human cells and then observing whether the inserted genes improve cellular function.
The other groups of investigators are affiliated with: the Buck Institute for Age Research in Novato, CA, studying the genetic causes of cell senescence (led by Dr. Judy Campisi); the Erasmus University Medical Center in Rotterdam, the Netherlands, developing biomarkers and studying interventions in DNA repair-defective mouse models (led by Dr. Jan Hoeijmakers); and the University of Texas Health Science Center in San Antonio, TX, also working with DNA repair-defective mouse models (led by Dr. Paul Hasty). Finally, the National Institute of Public Health and the Environment, in Bilthoven, the Netherlands, harbors the central core facility with all the mouse models kept under standardized, germ-free conditions (led by Dr. Harry van Steeg).
The information developed by the Einstein project may help to unravel one of the major mechanisms through which we age, which in turn may lead to new approaches to intervene on a rational basis. "Ultimately," says Dr. Vijg, "our hope is that this research will lead to new strategies that can be deployed for delaying, preventing, or even curing age-related disease."
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http://www.einstein.yu.edu/home/news.asp?id=401
NIH Awards Einstein $3.5 Million To Study Epigenomics Of Human Health And Disease
September 17, 2009 — (Bronx, NY) — The National Institutes of Health (NIH) has awarded Albert Einstein College of Medicine of Yeshiva University two grants totaling $3.5 million to study epigenetic changes — chemical modifications of genes caused by stress, diet or other environmental influences — and how they contribute to human diseases and biological processes.
The NIH will award approximately $62 million to medical institutions over the next five years to study the impact of epigenetic changes on a number of diseases and conditions, including tumor development, hardening of the arteries, autism, glaucoma, asthma, aging, and abnormal growth and development. The grants will build on the work of the NIH Roadmap for Medical Research's Epigenomics Program.
Einstein's grants will focus on epigenetic modifications related to abnormal fetal growth and to chronic kidney disease, led, respectively, by Francine H. Einstein, M.D., assistant professor of obstetrics & gynecology and women's health and Katalin Susztak M.D., Ph.D., associate professor of medicine. Their research will illuminate the total repertoire of epigenetic influences — referred to as the "epigenome"— that characterize each of these conditions.
"The goal of epigenomics research is in part to understand how human diseases are caused and how environmental factors affect them," says John M. Greally, M.B., B.Ch., Ph.D., associate professor of genetics and of medicine at Einstein, who directs Einstein's Center for Epigenomics. "This research is also driven by the fact that epigenetic processes are inherently reversible and could therefore respond to therapies that reverse long-term damage to the cells. These pioneering studies by Drs. Einstein and Susztak are the first steps towards this ultimate goal."
"Epigenomics represents the next phase in our understanding of genetic regulation of health and disease," says NIH Director Francis Collins, M.D., Ph.D. "These awards will address the extent to which diet and environmental exposures produce long-lasting effects through changes in DNA regulation." Dr. Collins notes that the initiative "is expected to profoundly alter the way we understand, diagnose and treat disease."
The main epigenetic modification being studied in these projects is DNA methylation, the addition of methyl groups to the cytosine bases of DNA, often associated with silencing of nearby genes. DNA methylation is one of a number of epigenetic regulatory mechanisms that control gene expression in normal cells but can become altered in disease. For example, epigenetic changes have been found in every type of cancer that researchers have studied.
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http://www.einstein.yu.edu/home/news.asp?id=416
Such a list does not exist, as I've been trying to tell you aging is a complex multi-factorial syndrome whose definition is not well defined. Genetic research will thus be extremely difficult, if not impossible to do in humans (unless you take extremes).bioquest said:I just want a list of the mutations that definitely contribute t aging in all individuals or @ least most individuals
A mutation is a change in the DNA sequence that can alter the function of a gene or protein. It can occur spontaneously or be induced by environmental factors such as UV radiation or chemical exposure.
Yes, mutations can potentially contribute to the aging process. As we age, our cells accumulate mutations in their DNA, which can lead to a decline in cellular function and overall health.
The most common mutations associated with aging are those that affect DNA repair mechanisms, telomere maintenance, and mitochondrial function. These mutations can result in increased DNA damage, shortened telomeres, and decreased energy production, which can all contribute to the aging process.
Not necessarily. While some mutations can contribute to aging, others may have a protective effect. For example, mutations that increase the expression of certain proteins involved in DNA repair can help counteract the effects of aging-related mutations.
While we cannot prevent aging-related mutations from occurring, we can potentially slow down their accumulation through healthy lifestyle choices such as a balanced diet, regular exercise, and avoiding harmful environmental exposures. Additionally, ongoing research is exploring ways to target specific mutations and potentially reverse their effects on aging.