For the First Time, Organ Regenerated Inside a Living Animal

ananyo (2519492) writes "Scientists at Edinburgh University have successfully persuaded an organ to regenerate inside an animal. As they report in the journal Development, they have treated, in mice, an organ called the thymus, which is a part of the immune system that runs down in old age. Instead of adding stem cells they have stimulated their animals' thymuses to make more of a protein called FOXN1. This is a transcription factor (a molecular switch that activates genes). The scientists knew from earlier experiments that FOXN1 is important for the embryonic development of the thymus, and speculated that it might also rejuvenate the organ in older animals. They bred a special strain of mice whose FOXN1 production could be stimulated specifically in the thymus by tamoxifen, a drug more familiar as a treatment for breast cancer. In one-year-olds, stimulating FOXN1 production in the thymus caused it to become 2.7 times bigger within a month. In two-year-olds the increase was 2.6 times. Moreover, when the researchers studied the enlarged thymuses microscopically, and compared them with those from untreated control animals of the same ages, they found that the organs' internal structures had reverted to their youthful nature."

Comments

All part of the plan

[bravehamster]

Those hyper-intelligent pan-dimensional mice sure are good at getting humans to do all the work to cure mice of all disease and aging.

Re:And the telomeres?

[Immerman]

Presumably the telomeres continue to diminish as normal; however, unless I'm much mistaken organisms rarely survive long enough for their cells DNA to run out of telemorase. Instead the problem is a far more complicated and poorly understood - some of aging happens at the cellular level, but far more happens at a system level, and we don't really understand the interaction. It sounds like they may have found a way to rejuvenate an organ at the system level, presumably at a some increase in aging at the cellular level (a 3x increase in size could well be responsible for less than 1.6 generations of cellular aging), but if we could extend lifespans such that it was generally cellular aging that killed us rather than systemic aging, that would be a pretty impressive leap forward. As a side benefit greater systemic health probably promotes greater cellular health, so we might end up with cells more like that spry centenarian happily working his farm rather than the decrepit 70yo who's doing good to wipe his own ass.