Aging is something that happens to everyone, but now, researchers believe they have found one of the key drivers behind the process. This finding could prove to have benefits in biology and medicine.
Werner syndrome is a rare disease marked by premature aging in victims. Victims often develop gray hair in their 20s, their eyes and bones start to fail in their 30s and they usually pass away before the age of 60. For the first time, researchers were able to create stem cells that carry the defect responsible for the tragic illness.
Relaxed DNA was found to be a driving force behind the disease in patients, and it could also be responsible for aging in healthy human beings as well, researchers report.
Hutchinson-Gilford Progeria Syndrome (HGPS) is an illness in which the physical characteristics of children morph to resemble senior citizens. Victims of this disease usually die by the time they are teenagers.
Medical researchers have long sought to understand whether the effects of HGPS and Werner syndrome were true aging or if the symptoms just resembled an accelerated form of the natural process. Stem cells were studied in an effort to determine the underlying causes of the diseases.
Genetic material in cells is often wrapped around proteins, producing a structure known as chromatin. Younger cells are capable of packing these items into orderly arrangements, called heterochromatin. Levels of heterochromatin were found to be lower in the teeth of adults, compared with children. This suggested to researchers that concentrations of the structures likely decline over time.
Mesenchymal stem cells (MSCs), which are the raw material of bone cells, cartilage and fat, were also found to be defective in patients suffering from Werner syndrome. When researchers crossed these MSC cells with embryonic stem cells, which can morph into any form, the cells began to age quickly and showed signs of DNA damage.
Other signs of aging include the shortening of telomeres that protect the tips of chromosomes and cells ceasing reproduction and falling into a state of stagnation known as cellular senescence. Medical researchers believe cells in this condition lead to tissues unable to replace themselves or heal from injury.
"This study provides evidence that abnormal chromatin structure ... is likely a major contributing factor to premature aging characteristic of the genetic disorder Werner syndrome ... defective chromatin organization may underlie normal aging as well," Robert Brosh, a molecular biologist from the National Institute on Aging, said.
This study could potentially lead to new ways of treating diseases that cause premature aging. However, it is unlikely to lead to longer lifespans — or immortality — for most people due to complications in altering levels of heterochromatin or clinching up genetic material.
Analysis of the role relaxed DNA plays in the aging process as well as Werner syndrome and HGPS was detailed in the journal Science.
Photo: Bùi Linh Ngân | Flickr
