Scientists have reached a milestone in the search for the Fountain of Youth by discovering a common foundation between aging and diseases.
The discovery by scientists at the Skaggs Institute for Chemical Biology of the Scripps Research Institute in La Jolla, California, and the Genomics Institute of the Novartis Research Foundation could be the springboard to drugs that keep our faces wrinkle-free.
"In order to come up with drugs, we need to understand [the aging] process. Before we didn't know where to aim our gun, but now we have a model," said Danith Ly, lead author of a study published Friday in Science that identified one common element in aging tissues throughout the body. "We've provided a general marker for identifying aging, and a model for explaining the process."
Until recently, researchers thought that cells stopped dividing as people aged. The study found, however, that cells continue to divide, but errors during the process cause the changes in our bodies associated with aging.
"Aging is a result of the misregulation of genes -- in a normal [and young] body, cell division is highly regulated by checkpoints," Ly said.
Checkpoints are like a border patrol, Ly explained, and DNA is like a car coming through. As we get older, there's no guard to check for illegal substances, so bad cells are bound to pass through. Hence we get wrinkles and our hair falls out.
The researchers examined 6,800 genes associated with aging by using DNA microarrays, or chips, to look at gene-expression patterns. The scientists placed bits of DNA from known genes on a fingernail-sized chip and exposed it to fluorescent light, highlighting the active genes.
Only 61 out of the 6,800 genes studied lit up, indicating that only a small number of genes are active in the aging process. That narrows the playing field for researchers.
"This takes us away from the picture that everything becomes dysfunctional with age," said Mike Mullan, director of the Roskamp Institute at the University of South Florida in Tampa. "It suggests that the major function of genes remains normal with age, and is not impaired. Clearly the genes that do change are going to be the critical ones."
The researchers looked at actively dividing fibroblast cells donated by young, middle-aged, and older patients. They compared the cells to each other, as well as to cells from patients with a rare disease called progeria, which causes accelerated aging and normally kills children in their teens.
Fibroblasts are the basis of all connective tissue in the skin, and about 95 percent are the same as our skin, bones, and hair, Ly said. Although the study was done on cells in culture, Ly said it's likely the same thing is happening in people.
"We can't study humans, but this is the closest you can get," he said.
The gene chip allowed researchers to look at the huge amounts of information the scientists needed to analyze, enabling them to see the big picture rather than just one gene at a time.
With the huge amounts of information being made available to scientists through the Human Genome Project, the chip technology promises to be the wave of the future in genetic research.
Mullan said that if other researchers use the chip technology and employ a similar model, it could mean big advances in the field.
"I think this is a key step in piecing together the aging process," Mullan said. "What's really nice about this work is we're not just looking at one gene or protein associated with age but [more than] 6,000, so you get an idea how aging as a coordinated mechanism is changing."
