The photo shows professor HAYASHI, the scientist who lead the study about aging. He is called ‘’White Lion’’ by his students because of his white hair and big voice. (CREDITS: TSUKUBA)

Aging is a natural process, most of the people “are afraid of”.

Deepak Chopra, once said “The only method of relieving yourself from aging is by reinterpreting you body and by grasping the link between belief and biology”.

However, new study shows that this is not the only manner of reversing aging. It seems that scientist now have the key of eternal youth.

Aging has always fascinated scientist and different theories have been published, but the Japanese study seems to be the Holy of the Medicine (for the reason that the experiments were done in human cells). In November 2010, Harvard University published an important study at ’’Nature’’ scientific journal showing reverse aging in mice. Specifically, the study showed that scientist could rejuvenate worn out organs in elderly mice.

The  Japanese team of the Tsukuba University, lead by professor Hayashi, proved that human aging may be able to be delayed or even reversed, at least at the most basic level of human cell lines. So far, all studies related to aging are focused on the mitochondria (Figure 1), the so-called powerhouse of the cell as it produces energy in a process called cellular respiration.

For the first time, Hayashi et al showed that aging can be reversed through regulation of two key genes, CGAT and SHMT2. The researchers' findings dispute the theory that mitochondrial defects are linked to mutation accumulations, and instead suggest they are caused by another form of genetic regulation.

Figure 1 shows Japanese noriben, in the shape of mitochondria –credits University of Tsukuba

Let’s explain this further. According to “The mitochondrial theory of aging” the main reason of aging is due to defects in the cell’s mitochondria. Just like nucleus, it is thought that mitochondrion contains some DNA. It turns out that mitochondrial DNA (mtDNA) gets mutations much faster than the DNA in the nucleus. One reason for this is thought to be the presence of ROS or "reactive oxygen species" (also known as "free radical") in the mitochondria. When mitochondria make energy for us, they create ROS that can damage nearby mtDNA. In fact, this might be the reason why eating less leads to longer lives in animals — less food, fewer ROS.

The idea is that as mtDNA becomes more and more damaged, the mitochondria cannot produce energy as well and become dysfunctional. This could lead to aging and ultimately, death.

The Tsukuba University proved that that the defects are not due to mutations in the DNA after all, but that external factors might be driving them. They looked at how the mitochondria were working in cell lines derived from young people, and compared them with cell lines derived from older people. What they found was fascinating. There were no observable differences in the number of mitochondrial DNA mutations between the older and younger cells. 

This led the researchers to study another form of genetic regulation, the epigenetic one, which factors (such as the addition of certain proteins to the mtDNA) might be creating the defects that cause the signs of aging. If this were the case – the researchers purposed – then “resetting” the cell lines to stem cells would correct and remove these epigenetic factors. When they tested this with the cell lines from the older people, this is exactly what they found. Quite amazingly, it seemed to turn the “old” cells back into “young” ones.

The scientists searched for genes associated with mitochondrial defects that can be controlled epigenetically. They found two main genes; CGAT and SHMT2.These genes control the production of GLYCINE– a particular amino acid. In their experiment, they bathed the cell line derived from a 97 year-old woman in glycine for ten days and after ten days they saw that the glycine restored the mitochondria’s ability to produce energy and reversed some age related defects. This suggests that glycine treatment can reverse the age –associated respiration defects in human cell lines.

This theory sheds new light on the future.

Who knows, maybe one day some of us will have the opportunity to be “Forever Young”. But this will start a new debate “Where they will all live?” This is a topic will not yet discuss.



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