
We may be closer to finding the fountain of youth, thanks to 15-year-old Afghan boy. It was learned he possessed a mutation in a gene responsible for the enzyme which is crucial in repairing DNA damage in cells. The genetic flaw caused him to age prematurely and die essentially of old age before completing puberty.
"What we say is [that] both are valid and that, in particular, damage to DNA contributes to aging," says Jan Hoeijmakers, a geneticist at the Erasmus Medical Center in Rotterdam, the Netherlands, and lead author of the study, which comprised teams from four different institutions in Europe and the U.S. "Damage accumulates ... but it is modulated by your genetic makeup. If you have better repair and/or slower metabolism, you age slower."
The boy was studied in the 1990's, when admitted to a hospital in the Netherlands. His condition, now known as XPF-progeroid syndrome resulted in aging prematurely causing death of old age while still in puberty. His symptoms included hypertension, hearing and vision loss, kidney failure, anemia and sensitivity to light.
Damage caused by exposure to ultraviolet light, x-rays, chemicals in food, cigarette smoke and other stimuli are repaired by XPF-ERCC1 endonuclease. This complex is created by the XPF enzyme combining with the protein ERCC1 which forms the complex. The defective gene does not allow the body to repair DNA damage.
This research led scientists to examine the question "Do we age as a result of damage acquired throughout our lifetimes, or do our genetic markers indicate when and how we will age. According to Jan Hoeijmakers, a geneticist at the Erasmus Medical Center in Rotterdam, both have bearing on the aging process.
"Damage accumulates ... but it is modulated by your genetic makeup. If you have better repair and/or slower metabolism, you age slower." "Our own respiration and metabolism," Hoeijmakers says, "produce constantly reactive oxygen species and other chemicals that have a tendency to react with and damage all sorts of cellular components [including] ... our DNA." Damaged DNA leads to cell death or dysfunction and "over time you lose cells, cells and organs do not function so well anymore and you gradually age."
Slowing aging and fighting age-related disease is a pertinent issue with the majority of the population aging. Aging is not a disease, but a natural process of life. Easing into being older while remaining healthful, can preserve our quality of life. Age related illness is likely to put a huge burden on the health care systems, both in terms of skyrocketing costs, and the current labor shortage of health care workers.
"If we would be able to reduce the induction of DNA damage by triggering the survival response to lower metabolism and allow less damage or by boosting repair or, perhaps, by adding protecting compounds in food or medication," he says, "the rate of DNA damage and consequently aging may be reduced."
Cited from Scientific American
Article by Nikhil Swaminathan