AN UNUSUAL experiment in which the blood supplies of old and young mice were bound together as if they were conjoined twins has boosted hopes of one day giving new life to old bodies.
A team led by of the Harvard Stem Cell Institute in Boston, Massachusetts, discovered that the blood of the young animals seemed to rejuvenate ageing blood stem cells in the bone marrows of the older mice. It also revitalised so-called 鈥渘iche鈥� cells in the bone marrow, which nourish, support and stimulate blood stem cells.
Although old mice make more blood stem cells and more niche cells than young mice, many are faulty and don鈥檛 repair the body as efficiently as the younger equivalents. 鈥淭he reason the old animals have too many is probably an attempt to compensate for these flaws,鈥� Wagers says. Old mice also make too many myeloid blood cells, which contribute to inflammation and the development of cancer, and too few lymphoid blood cells, which orchestrate tissue repair.
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But when Wagers鈥檚 team yoked 21-month-old mice to young mice just 2 months old, all these age-related changes were reversed: the mice made fewer myeloid cells and more lymphoid cells (Nature, ). The researchers conclude that as-yet-unidentified components in the young mice鈥檚 blood passed into the older animals and prompted these youth-giving changes.
鈥淭he young mice鈥檚 blood flowed into the older animals, prompting youth-giving changes鈥�
Based on further experiments, Wagers suspects these blood components may prompt the repair of the old mice鈥檚 worn-out cells by blocking a hormone called insulin-like growth factor 1, which has been implicated in the ageing process. IGF-1 accelerated ageing in mouse niche cells, as the team expected, and when the researchers injected antibodies that neutralise IGF-1 into the bone marrows of old mice, the niche and stem cells remained young.
It鈥檚 not safe, though, to slow ageing in old people by injecting antibodies into the bone marrow that neutralise IGF-1, says Wagers. That鈥檚 because IGF-1 is vital for muscle and bone growth and antibodies might leak into the rest of the body. Instead, her team is now looking for a way to block the chemical signal that switches on IGF-1 production, exclusively in the bone marrow.
Attempting to slow ageing using blood transfusions from young people, to mimic more directly what happened in the yoked mice, is also out, says Wagers. A 鈥渙ne-off鈥� exposure to the relevant blood factors won鈥檛 reverse ageing, it would need to be constant.
