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One Step Closer toward Reversing Age, and One Step Further from Death?
Humanity has always grappled with the idea of mortality and has always tried to cope with aging. But recently, researchers advanced the battle against aging when a study discovered a new mechanism behind growing older. Researchers are particularly focused on this mechanism because, unlike others, it is reversible. Harvard Medical School, the National Institute on Aging, and the University of New South Wales revealed injecting a certain molecule that is naturally-occurring in humans into older mice reversed some signs of aging—so much that the older mice’s treated tissue resembled the tissue of six-month old mice.
The body’s gradual deterioration wreaks havoc on the mitochondria, cellular structures that produce energy in the form of ATP, or adenosine triphosphate. Without mitochondria, known as “powerhouses” of the cell, cells cannot function. In fact, if the mitochondria fail, so will the cell. While the cell’s nucleus has a genome that dictates all the cell’s activities, the mitochondria have their own genome as well. So, mitochondrial maintenance requires proper communication between the two genomes. These new findings suggest that an issue with mitochondria is the gradual decay of communication between the nucleus and the “powerhouse,” rather than previously-held presumptions that mitochondrial genomic mutations are the root of many age-related conditions. When this communication becomes clouded, mitochondria eventually begin failing to produce appropriate energy, and signs of aging emerge.
The main players in this mechanism are the molecules NAD and HIF-1 and the gene SIRT1. Ana Gomes and her team in the Sinclair lab traced a biochemical pathway in the aging process, beginning with NAD and concluding with a molecule that harmonizes the nucleus and the mitochondria. When these two structures efficiently communicate, the cell is often healthy. HIF-1 is the major culprit in clogging this line of communication not only in aging, but also in oxygen deprivation and cancer. So, to prevent HIF-1 from building up, SIRT1, part of a family of genes referred to as sirtuins, maintains the biochemical pathway between the nucleus and mitochondria. Gomes tested SIRT1’s role by deleting the SIRT1 gene from mice; this deletion caused significantly more aging in experimental mice than in normal mice.
So what goes wrong during aging? For some still unknown reason, the prevalence of NAD plummets with age. When NAD declines, so does SIRT1’s capacity to track HIF-1, allowing HIF-1 to build up and to intrude on the pathway, interfering with communication and facilitating aging. Fortunately, communication, unlike genetic mutations, can improve when given the right tools. Gomes tested a solution on mice; inserting a precursor to NAD into older mice patched up the communication network, and if she administered the injection before too many mitochondrial mutations set in, the reintroduction of NAD reversed some signs of aging, including inflammation, muscle wasting, and resistance to insulin.
Uncovering this mechanism also takes a step closer to solving many age-related illnesses like Diabetes or Alzheimer’s, as well as mitochondrial diseases. Moreover, because previous studies suggest that cancer increases HIF-1, this research may also have a future role in cancer treatment and prevention. These findings have many implications, which may one day give many people solace.
Rhiana Simon, Contributor