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Aging – is it reversible ?

Aging always was a subject of scientific interest. How and why aging processes are happening? Is it possible to control the aging process? How to turn off cell aging?

Scientists from the University of Tsukuba found that the aging of human cells can be slowed or even reversed. They identified two genes whose function is associated with the aging mechanisms. It is well known that human body cells get their energy through specific “organelles” located inside the cells (so called “mitochondria”). It is assumed that at the beginning of the evolution of anaerobic cells (which are unable to absorb oxygen) merged into a symbiotic partnership with ancient bacteria that are able to do so. As a result, mitochondria lost their independency and become just energy source for cells – they serve as cells’ energy “factory”.

Aging – scientific theories and new opportunities

Human aging and transformation of human cells is the subject of numerous scientific studies. According to popular theory, on-going use of mitochondria energy is triggering mitochondrial constant division and gradual accumulation of mutations in mitochondrial DNA. As a result, mitochondria become “spoiled” and their energy power (properties) gradually depleted. Later scientists suggested that damage of mitochondria could be done by free radicals.

Researchers from Tsukuba University suggested that the key is not in “spoiled” mitochondrial DNA but over time certain genes begin turn on and off. Scientific team of Professor Jun-Ichi Hayashi was able to switch certain genes in the “youth” mode and reverse the aging.

Aging - is it reversible

Aging – is it reversible

In their study, the researchers compared the fibroblasts (human connective tissue cells) of children under the age of 12 years and the elderly from 80 to 97 years. Naturally, in the cells of the elderly the significant decrease in cellular respiration was noted. Cellular respiration is a set of biochemical reactions in the cells – oxidation of carbohydrates, lipids and amino acids into carbon dioxide and water. Actually researchers didn’t note any significant DNA damage in the mitochondria of elderly people. This is why scientists suggested that most probably the main responsible mechanisms are related to epigenetic effects that alter the activity of genes – as a result certain genes “turned on” and the others “turned off.” This means that it is theoretically possible to reverse epigenetic DNA changes by reprogramming cells.

First, scientists collected stem cells. Second, they reprogrammed collected cells. Third, scientists turned reprogrammed cells into fibroblasts. The result of the experiment was shocking – all cells cellular respiration was restored to the regime of “youth”.

That was a start of research on reversible aging. Therefore, the researchers began the search for genes that can be switched in order to prevent the aging of cells. They found two genes, GCAT and SHMT2, which regulate the synthesis of the glycine – amino acids produced by the mitochondria.

It was found that by adjusting the operation of these genes, it was possible to completely “rejuvenate” mitochondria in cells. In experiment, adding the glycine to the culture of cells of older people (during 10 days) leads to the full restoration of fibroblasts’ cellular respiration.

Based on mentioned scientific studies, researchers from Tsukuba University concluded that contrast to the current theory of aging, the fibroblast cellular respiration defects are caused by certain epigenetic processes. Is it possible, by adjusting these processes, manage the mechanisms of becoming older?

Professor Jun-Ichi Hayashi, University of Tsukuba, Japan

Professor Jun-Ichi Hayashi, University of Tsukuba, Japan

“In contrast to the well-known theory of aging, which places the entire responsibility on the damaging mutations; epigenetics opens new opportunities for cell reprogramming – reversing cells from aging mode (status) to the state of youth. In fact, there is a revolutionary scientific opportunity to turn back the clock.”
Professor Jun-Ichi Hayashi, University of Tsukuba, Japan


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