Scientists Reverse Aging in Human Cell Lines; Epigenetic Regulation, Not Mutations, Appears to Determine Age-Associated Defects in Mitochondria; Work Suggests Glycine Treatment May Reverse Age-Associated Mitochondrial Respiration Defects in Elderly

Can the process of aging be delayed or even reversed? Research led by specially appointed Professor Jun-Ichi Hayashi (photo) from the University of Tsukuba in Japan has shown that, in human cell lines at least, it can. They also found that the regulation of two genes involved with the production of glycine, the smallest and simplest amino acid, is partly responsible for some of the characteristics of aging. Professor Hayashi and his team made this exciting discovery while in the process of addressing some controversial issues surrounding a popular theory of aging. This theory, the mitochondrial theory of aging, proposes that age-associated mitochondrial defects are controlled by the accumulation of mutations in the mitochondrial DNA. Abnormal mitochondrial function is one of the hallmarks of aging in many species, including humans. This is mostly due to the fact that the mitochondrion is the so-called powerhouse of the cell as it produces energy in a process called cellular respiration. Damage to the mitochondrial DNA results in changes or mutations in the DNA sequence. Accumulation of these changes is associated with a reduced lifespan and early onset of aging-related characteristics such as weight and hair loss, curvature of the spine and osteoporosis. There is, however, a growing body of conflicting evidence that has raised doubts about the validity of this theory. The Tsukuba team in particular has performed some compelling research that has led them to propose that age-associated mitochondrial defects are not controlled by the accumulation of mutations in the mitochondrial DNA but by another form of genetic regulation.
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