The Pursuit For Longevity: Harvard Scientists Discovers How To Reverse Aging [Video]


Aging does not just affect the body aesthetically but most of all, it greatly impacts how the body heals itself. This is the reason why scientists are putting in hours of research and study how to reverse aging. And they might be at the threshold of perpetual youth as a group of Harvard scientists claimed just recently.

A group of scientists from Harvard Medical School recently announced that they have discovered a very important step in reversing the process of aging. This process allows cells to heal and mend broken DNA. This process involved the interactions of different important proteins in the body.

Proteins In The Aging Process

There are four components that play an important role in aging - the molecule NAD, and the proteins SIRT1, PARP1, and DBC1.

NAD, a signaling molecule, had been identified a long time ago as the key regulator of how proteins interact with each other in the DNA repair process. NAD, specifically controls cell-damaging oxidation.

SIRT1 is a protein that delays aging and extends the life in mice, yeast, and other flies. PARP1, on the other hand, is a protein that controls DNA repair. These proteins bond together and consume NAD in their work.

The problem, however, lies when DBC1 bonds with either SIRT1 or PARP1. Previous studies showed that when DBC1 bonds with SIRT1, it inhibits the vitality-boosting power of SIRT1. This led the scientists to think that DBC1 might also be affecting PARP1.

Their hunch was correct because DBC1 and PARP1 indeed bond and with lethal consequences. The more these two proteins bond, the more DNA damages go unrepaired. As they grow over time, more and more cells get damaged and die resulting in organ failures.

Reversing the Aging Process

Aside from observing the deadly bonding, the scientists also found out that if they increased the levels of NAD, the DBC1 and PARP1 bonding is disrupted. They also discovered that when they block the NHD region with NAD, DBC1 is prevented from locking with PARP1.

NHD is a pocket-like structure that is present in more than 80,000 kinds of proteins that exist in all organisms including humans.

What the scientists did was treat old mice with NMN, a NAD precursor. Once they are inside the body, an NMN bonds with another NMN to become a NAD. After several weeks of treating old mice with NMN, they showed progress and improved activity similar to younger mice. This led them to suggest that NMN treatment should be explored further to see more impact on cellular repair.

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