Health scientists at the Harvard Medical School in America have managed to reverse the ageing process in animals. A newly designed chemical was injecting into the muscle tissue of mice and the effect was the equivalent of transforming a 60 year-old’s muscle into that of a 20-year-old.
The research was published in Cell and looked at one specific form of ageing. In fact, the researchers had first discovered a new type of cellular ageing and then managed to reverse the process.
The research examined the role of a chemical called NAD which occurs naturally in the body but declines as we grow older.
When two-year-old mice were injected with the chemical their muscles repaired and renewed until they became like those of a 6 month old mouse. The key indicators for recovery were improvements in mitochondrial function, muscle wastage, inflammation and insulin resistance.
Muscle strength did not return immediately, but Dr Ana Gomes, from the department of genetics at Harvard Medical School, believes that in time muscle strength will recover. The muscle cells will have the capacity to grow stronger again, a capacity which was lost during ageing.
Can it really reverse ageing?
Unfortunately building younger muscles is only one facet of being youthful. As we age there is increased DNA damage and reductions in cardiovascular fitness. To really be young again every cell would have to be renewed in a similar way.
It may be possible for scientists to discover how to do this one day, but for the time being the research is not going to help old people spring back to life again. This is certainly not the technology seen in Cocoon!
This is certainly an exciting piece of research which hints that it is indeed possible to reverse the ageing process. You cannot help thinking that it is just a matter of time before we are able to halt or reverse the ageing process completely. The only problem is, unlike the characters from Cocoon, we will not have the luxury of retiring early, instead we will all be working well into our hundreds.
Declining NAD+ Induces a Pseudohypoxic State Disrupting Nuclear-Mitochondrial Communication during Aging by Ana P. Gomes et al in Cell, Volume 155, Issue 7, 1624-1638, 19 December 2013. 10.1016/j.cell.2013.11.037
Ever since eukaryotes subsumed the bacterial ancestor of mitochondria, the nuclear and mitochondrial genomes have had to closely coordinate their activities, as each encode different subunits of the oxidative phosphorylation (OXPHOS) system.
Mitochondrial dysfunction is a hallmark of aging, but its causes are debated. We show that, during aging, there is a specific loss of mitochondrial, but not nuclear, encoded OXPHOS subunits.
We trace the cause to an alternate PGC-1α/β-independent pathway of nuclear-mitochondrial communication that is induced by a decline in nuclear NAD+ and the accumulation of HIF-1α under normoxic conditions, with parallels to Warburg reprogramming.
Deleting SIRT1 accelerates this process, whereas raising NAD+ levels in old mice restores mitochondrial function to that of a young mouse in a SIRT1-dependent manner.
Thus, a pseudohypoxic state that disrupts PGC-1α/β-independent nuclear-mitochondrial communication contributes to the decline in mitochondrial function with age, a process that is apparently reversible.