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A recent finding by scientists from the Hospital for Sick Children, Toronto, and Duke University challenges long-held ideas about why our bones have a harder time healing as we age. Their research discovered that old mouse bones mend like youthful bones do when they’re exposed to young blood after a fracture.

“The traditional concept is that as you get older, your bone cells kind of wear out so they can’t heal as well, and we thought we’d find that during this study as well,” explains study co-author Benjamin Alman, of the Hospital for Sick Children. “But it turns out that it’s not the bone cells, it’s the blood cells. As you get older, the blood cells change the way they behave when you have an injury, and as a result the cells that heal bone aren’t able to work as efficiently.”

The researchers paired lab mice, one old and one young, and subjected them to bone fractures, but that wasn’t all they had in common. The living animals’ circulatory systems were also joined together by a 150-year-old surgical technique known as parabiosis. Scientists removed a layer of skin from each mouse and stitched the exposed surfaces together. As the animals healed their capillaries joined, enabling their two hearts to pump the same blood throughout the two bodies as a single system. Parabiosis, which has been gaining new popularity in aging research, allowed Alman and colleagues to see what impacts the circulating factors of the younger mouse’s blood had when introduced into the body of an older mouse.

The experiment, published this week in Nature Communications, suggests that young blood cells secrete some as-yet-unknown molecule, likely a protein or possibly some other chemical, that speeds up the healing of fractured bone. The molecule apparently does so by regulating levels of beta-catenin in bone cells known as osteoblasts. Keeping beta-catenin at the proper levels appears crucial for the formation of new high-density bone.

This ability is greatly diminished in older animals’ blood because it no longer secretes the molecule, whose exact chemical nature remains a mystery at this point. “My guess is that there are a number of proteins involved that are made differently as we get older, and that they are responsible for the difficulty in healing bone,” Alman says.

The findings could prove good news for aging humans, but healing our bones won’t require the type of transfusions used in the experiment—nor will it borrow the synthesized “True Blood” variety that may soon enter clinical trials. Sharing human blood in this manner raises a number of red flags ranging from practicality to possible medical complications.

Source: www.smithsonianmag.com

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