The question about whether it is possible to reverse ageing has been with us for some time. Recent research by the University of Tsukuba in Japan, and led by professor Jun-Ichi Hayashi, has shown that it can be within human cell lines.
Current theory around aging says, age-associated mitochondrial defects are controlled by the accumulation of mutations in the mitochondrial DNA. This mitochondria behaviour is a sign of ageing in humans and other species. This is because mitochondrion represents the power within the cell through a process called cellular respiration. When the mitochondrial DNA is damaged it creates changes in the DNA sequence. When these changes build up they are linked to the onset of aging, including hair loss and spinal curvature.
There is growing evidence that places doubt on this theory. The team from Tsukuba recent research has suggested age-associated mitochondrial damage aren’t effected by mutations in the mitochondrial DNA but by a different form of genetic control.
The research compared the performance of mitochondria in humans 0-12 and 80-97 years old. They compared the mitochondrial respiration to the DNA damage in the two groups of mitochondria. They expected respiration to be less in the older age group, but whilst it was reduced there was no difference in the DNA damage between young and old.
The researchers then thought they would check a different form of regulation and explored epigenetic regulation, and think this may now be responsible for changes in the mitochondria. Epigenetic regulation relates to the addition of chemical structures that change the physical structure of DNA which turns genes on or off. These changes do not effect the DNA sequence as mutations do. If this research theory is correct, then reprogramming cells to an embryonic stem cell–like state would remove any epigenetic changes associated with the mitochondrial DNA.
The tests undertaken involved reprogrammed human fibroblast cells, taken from both older and younger people, to an embryonic stem cell-like state. The cells were then turned back to fibroblasts so the mitochondrial respiratory function could be examined. Amazingly age related defects had been reversed, irrespective of whether they were taken from young or old, all of the fibroblasts had respiration rates comparable to those of the fetal fibroblast cell line.
It was found that the addition of glycine for a 10 day period to the fibroblast cell line from 97 year olds restored its respiratory function. This indicated to the team that age related respiration defects in older human fibroblasts can be treated with glycine.
The research shows that contrary to mitochondrial theory, epigenetic regulation effects age-associated respiration defects in human fibroblast cell lines. We have to wait and see whether epigenetic regulation can control ageing in humans but if it can, get ready for glycine supplements to give a lease of new life to the elderly.