Chinese and US researchers working on a premature aging disorder said at the end of April that changes in heterochromatin, a tightly packed form of DNA, could be blamed for the aging process in humans.

The findings, made possible through a combination of cutting-edge stem cell and gene-editing technologies, could lead to methods of preventing and treating age-related diseases such as cancer, diabetes and Alzheimer's disease, the researchers reported in the US journal Science.

"We proposed a new theory that suggests the disorganization of heterochromatin is a key driver of human stem cell aging," said senior author Liu Guanghui of the Institute of Biophysics at the Chinese Academy of Sciences in Beijing.

Liu called their work "an important supplement" to current aging theory, which proposes that aging is a consequence of the accumulation of naturally occurring DNA damage.

In the study, scientists at the Salk Institute and the Chinese Academy of Sciences looked at Werner syndrome, a genetic disorder that causes people to age more rapidly than normal.

Werner syndrome affects around one in every 200,000 people in the United States. People with the disorder suffer age-related diseases early in life, including cataracts, type II diabetes, hardening of the arteries, osteoporosis and cancer, and most die in their late 40s or early 50s.

The disease is caused by a mutation to the Werner syndrome RecQ helicase-like gene, known as the WRN gene for short, which generates the WRN protein, so the researchers created a cellular model of Werner syndrome by using a cutting-edge gene-editing technology to delete the WRN gene in human stem cells.

The resulting cells mimicked the genetic mutation seen in Werner syndrome patients, so the cells began to age more rapidly than normal. On closer examination, the researchers found that the deletion of the WRN gene led to disruptions to the structure of heterochromatin, pointing to an important role for the WRN protein in maintaining heterochromatin.

In further experiments, they showed that the protein interacts directly with molecular structures known to stabilize heterochromatin, revealing a kind of smoking gun that, for the first time, directly links mutated WRN protein to heterochromatin destabilization.

Finally, they compared stem cells isolated from six young and six elderly individuals and found a marked downregulation of WRN protein and a decrease in the level of heterochromatin derived from old individuals, further suggesting that accumulated alterations in the structure of heterochromatin may be a major underlying cause of cellular aging.

"This has implications beyond Werner syndrome," senior author Juan Carlos Izpisua Belmonte of the Salk Institute said in a statement. "It identifies a central mechanism of aging－heterochromatin disorganization－which has been shown to be reversible."

Belmonte said more studies would be needed to fully understand the role of heterochromatin disorganization in aging, including how it interacts with other cellular processes implicated in aging.