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Scientists from Harvard and the University of New South Wales say they have discovered how to reverse the ageing process.
The research has focused on mice, but early clinical trials have also been conducted on humans.
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"We fed them a molecule that's called NMN and this reversed ageing completely within just a week of treatment in the muscle, and now we're looking to reverse all aspects of ageing if possible."
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"We've gone from mice into early human studies actually. There have been some clinical trials around the world, and we're hoping in the next few years to know if this will actually work in people as well," he said.

The clinical trials were small studies but showed promising results in humans, he said.

"They show that the molecules that extend lifespan in mice are safe in people; they seem to be anti-inflammatory, so they might be useful against disease's inflammation, like skin redness or even inflammatory bowel disease," he said.
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He has been taking the red wine molecule, resveratrol, for a decade.

"I've been taking resveratrol for the last 10 years because it seemed to be very safe," he said.

"I think the risks are, for myself, worth it, though I don't ever promote it.
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A rise in NAD precursor nicotinamide mononucleotide (NMN) after injury promotes axon degeneration

Abstract
NAD metabolism regulates diverse biological processes, including ageing, circadian rhythm and axon survival. Axons depend on the activity of the central enzyme in NAD biosynthesis, nicotinamide mononucleotide adenylyltransferase 2 (NMNAT2), for their maintenance and degenerate rapidly when this activity is lost. However, whether axon survival is regulated by the supply of NAD or by another action of this enzyme remains unclear. Here we show that the nucleotide precursor of NAD, nicotinamide mononucleotide (NMN), accumulates after nerve injury and promotes axon degeneration. Inhibitors of NMN-synthesising enzyme NAMPT confer robust morphological and functional protection of injured axons and synapses despite lowering NAD. Exogenous NMN abolishes this protection, suggesting that NMN accumulation within axons after NMNAT2 degradation could promote degeneration. Ectopic expression of NMN deamidase, a bacterial NMN-scavenging enzyme, prolongs survival of injured axons, providing genetic evidence to support such a mechanism. NMN rises prior to degeneration and both the NAMPT inhibitor FK866 and the axon protective protein WldS prevent this rise. These data indicate that the mechanism by which NMNAT and the related WldS protein promote axon survival is by limiting NMN accumulation. They indicate a novel physiological function for NMN in mammals and reveal an unexpected link between new strategies for cancer chemotherapy and the treatment of axonopathies.