Young blood has once again shown its promise as an elixir of youth: blood from young mice helps bones of older animals heal.
Over the past few years, researchers have reversed muscle atrophy, memory loss, heart degradation and some of the effects of cognitive decline by pumping the blood of young mice into old mice. The results from these animal experiments were so intriguing that last year a team at Stanford University began the ultimate rejuvenation trial: giving blood plasma from under 30s to people with Alzheimer’s. Results are expected next year.
Now, Benjamin Alman, a professor of surgery at the Hospital for Sick Children in Toronto, Canada, and his colleagues have tested young blood’s ability to heal bones.
The team surgically joined the circulatory systems of mice of various ages, in a procedure known as parabiosis. Fractured shin bones of old mice healed faster and better when the rodents were joined to young mice than to mice their own age.
Nature Communication – Exposure to a youthful circulaton rejuvenates bone repair through modulation of β-catenin
12 pages of supplemental information
The capacity for tissues to repair and regenerate diminishes with age. We sought to determine the age-dependent contribution of native mesenchymal cells and circulating factors on in vivo bone repair. Here we show that exposure to youthful circulation by heterochronic parabiosis reverses the aged fracture repair phenotype and the diminished osteoblastic differentiation capacity of old animals. This rejuvenation effect is recapitulated by engraftment of young haematopoietic cells into old animals. During rejuvenation, β-catenin signalling, a pathway important in osteoblast differentiation, is modulated in the early repair process and required for rejuvenation of the aged phenotype. Temporal reduction of β-catenin signalling during early fracture repair improves bone healing in old mice. Our data indicate that young haematopoietic cells have the capacity to rejuvenate bone repair and this is mediated at least in part through β-catenin, raising the possibility that agents that modulate β-catenin can improve the pace or quality of fracture repair in the ageing population.
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