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Researchers discover cause of aging that may be reversible

Category: DNA, Paternity and Genetic testing

Findings published in the December issue of Cell detail the astounding results from lab tests conducted to determine the cause of aging in mammals. Led by David Sinclair, Ph.D, the team was able to restore cell communication pathways that breakdown and essentially discovered a possible method of reversing the aging process.

"The aging process we discovered is like a married couple - when they are young, they communicate well, but over time, living in close quarters for many years, communication breaks down. And just like with a couple, restoring communication solved the problem," explained Sinclair, professor of genetics at Harvard Medical School in Boston, Mass.

Inside cells, mitochondria carry out essential functions for the body by generating chemical energy and communicating with the nucleus. As this cellular conversation breaks down, the process of aging begins to accelerate. This dysfunction of cells is what causes age-related medical conditions such as diabetes and Alzheimer's disease. According to the team, scientists have always been hesitant to believe the effects of getting physically older could be reversed due to the theory that these diseases centered around aging are the result of irreversible mutations at the genetic level.

Working with SIRT1
The scientists found that one gene in particular, called SIRT1, was an important piece of the genetic puzzle of aging. To test the importance of SIRT1, the researchers studied mice whose SIRT1 gene had been removed. While the mice showed dysfunction of the mitochondria and other signs of aging, they were shocked to discover that many of the proteins coming from the nucleus of the cell were normal. Through further investigation, their research revealed a significant breakdown between the genomes of the cell's nucleus and mitochondria, with SIRT1 acting as a guard to prevent any interference in communication. Without it, the cells lose their ability to make energy and signs of aging and disease become prevalent. Sinclair's team was able to stabilize this breakdown with a compound that repairs the broken network and restores mitochondrial function.

After administering the compound for just one week, Sinclair's team found that the mice's insulin resistance, muscle wasting and inflammation instances had resemblance to that of 6-month-old mice. To equate this to human years, it is as if a 60-year-old converted to a 20-year-old.

"There's clearly much more work to be done here, but if these results stand, then many aspects of aging may be reversible if caught early," Sinclair concluded.

Now, the researchers are examining the long-term effects of their compound and how it affects the entirety of the mouse. They plan to test the compound further to determine if it can potentially extend the life of the mice.