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Buildup of damaged DNA in cells drives aging

es currently favored in the field of aging research about why we get old, according to the authors. The first is that our lifespan and how well we age is determined by the genes inherited from our parents. The second is that lifespan and fitness in old age is determined by how much damage we incur over our lifetime.

"Our study suggests that both of these hypotheses are correct. Damage, including DNA damage, drives the functional decline we all experience as we age. But how we respond to that damage is determined genetically, in particular by genes that regulate the growth hormone and insulin pathways," said Laura Niedernhofer, M.D., Ph.D., assistant professor of molecular genetics and biochemistry, University of Pittsburgh School of Medicine, and first author of the study.

How the researchers came to study the relationship between DNA damage and aging began almost serendipitously in the late 1990s while Dr. Niedernhofer was a post-doctoral fellow in Dr. Hoeijmakers?laboratory at Erasmus Medical Center, a well-known European center for medical genetics, including the diagnosis of people with unusual sensitivity to sunlight.

A German physician had contacted the center about a 15-year old Afghan boy who was highly sensitive to the sun and had other debilitating symptoms including weight loss, muscle wasting, hearing loss, visual impairment, anemia, hypertension and kidney failure. The boy’s family had immigrated to Germany to seek better medical treatment for his condition.

Extreme sensitivity to ultraviolet (UV) radiation from sunlight is a hallmark of diseases caused by defective DNA repair—an important mechanism by which skin and other cell types normally cut out, or excise, damage to their DNA caused by UV light. Defects in one DNA repair mechanism, nucleotide excision repair (NER), causes xeroderma pigmentosum, a rare disease in which people have a 2,000-fold increased risk of skin cancer from sun exposure.

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Source:University of Pittsburgh Medical Center


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