This popular science article looks at some of the present outcomes of heterochronic parabiosis research, in which the circulatory systems of two animals are linked, one older, one younger. This produces beneficial effects in the older animal, in particular a reactivation of stem cell populations and greater tissue maintenance. While some research groups are chasing down the molecular signals responsible, others are attempting to see if blood transfusions from young donors to old recipients could recapture any of the effect.
Personally I'm not optimistic with regard to the direct approach of transfusions based on the null results obtained from experiments in mice carried out to date. It is quite possible that the useful factors are very short-lived, or that the beneficial processes involved in heterochronic parabiosis require some interaction between old tissue and young tissue, and in either case straightforward transfusions of young blood are not going to be useful. Even when a method of recapturing parabiosis benefits is produced, as I'm sure it will be sooner or later, this still only partially addresses one of the causes of degenerative aging. Researchers still need to clear out metabolic waste, address mitochondrial damage, and so forth - the rest of the slate of SENS rejuvenation therapies are required.
On an August morning in 2008, Tony Wyss-Coray sat in a conference room at the Veterans Affairs hospital in Palo Alto, California, waiting for his lab's weekly meeting to begin. Saul Villeda, an ebullient PhD student with slick black hair and a goatee, had spent the past year engrossed in research that called to mind the speculative medical science of the middle ages. He was investigating whether the old and frail could be rejuvenated by infusions of blood from the young. Villeda had conducted pilot studies with pairs of surgically conjoined mice that shared a blood supply for several weeks. Young mice received blood from older mice, and old mice received blood from younger ones.
Villeda got three hours' sleep that night. The next morning, he stood up at the lab meeting and revealed to his colleagues what young blood did to the ageing brain. "There was a palpable electricity in the room," Wyss-Coray recalled. "I remember seeing the images for the first time and saying, 'Wow.'" Old mice that received young blood experienced a burst of brain cell growth in the hippocampus. They had three to four times as many newborn neurons as their counterparts. But that was not all: old blood had the opposite effect on the brains of young mice, stalling the birth of new neurons and leaving them looking old before their time.
Since that meeting seven years ago, research on this topic has moved on dramatically. It has led some to speculate that in young blood might lie an antidote to the ravages of old age. But the apparent rejuvenating properties of young blood must be treated with healthy scepticism. The hopes they raise rest solely on mouse studies. No beneficial effects have ever been proven in humans. Then again, no one has ever looked. That is about to change. In October 2014, Wyss-Coray launched the first human trial of young blood. At Stanford School of Medicine, infusions of blood plasma from young people are being given to older people with Alzheimer's disease. The results are expected at the end of the year. It is the greatest test yet for the medical potential of young blood.
Big questions lie ahead. Even if none of the patients benefit from young plasma, the research is far from finished. The plasma for the trial comes from donors under 30, and it may not be potent enough. The patients on the trial have dementia already, and may be too far gone to rescue. Earlier this year, John Hardy of University College London, who is the most cited Alzheimer's researcher in Britain, saw Wyss-Coray's latest data at a meeting in London. "It's really interesting work," he told me. "It's woken everybody up." Nonetheless, Hardy is cautious; he suspects that young plasma will be less effective in people than in mice, because people live so much longer, and in far more varied environments. But, he said: "I would guess this will still point us towards pathways involved in ageing more generally."