A New Development In The Quest For Mouse Immortality

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A study in mice shows that if you kill off aging, poorly-functioning cells in mice, the mice become healthier, more attractive, and more fun to be around. This is obviously the key to human immortality — as long as it doesn't kill us.


USA Today reports on the research, originally published in Nature. Scientists used a genetic tracer to find "senescent" cells — those that were no longer working right as a result of age. Then they used a drug to activate a "suicide gene" in these cells, making them die instead of sticking around. Result, according to Dr. Gary Kennedy, who read the research: "When they blocked the senescent cell process in mice prone to premature aging, they blocked the development of spinal arthritis, the loss of muscle, thinning of skin — they were all reversed. Mice that should have looked prematurely aged were essentially normal." The mice were also more active than usual. The treatment was most effective when it started at birth, but it also worked to some degree when started after the mice began to age.

Obviously, this is the Fountain of Youth. There's just one teensy little problem. Says Dr. Julian Sage, "The tricky part in people will be how many senescent cells you can eliminate without killing the person." There's no mention of whether any mice died as a result of the treatment, but researchers would presumably have to be quite careful when applying the technique to humans — you can't just go triggering a "suicide gene" all willy-nilly. It's also hard to study mouse personality, so it's not clear whether killing off all their old cells drove them crazy, or made them all vain and prissy, or caused the little mouse-portraits in their attics to age in their stead.

Clearing Out 'Old Cells' May Make For A Healthier Old Age [USA Today]


Stephan Zielinski

Ooh, pointer to the abstract, AND you've scooped IO9! That's gotta be worth some points.

Regarding that "suicide gene": in this case, Baker el alia had to design IN a gene that would result in cell death upon administration of a particular drug if-and-only-if the cell in question was senescent. (They named the new gene INK-ATTAC, where INK presumably comes from the biomarker for senescence they used as a trigger: p16INK4a.) Neither regular mice nor humans have it, and developing and putting one in would take some unprecedented fiddling with people's genetic code. Not necessarily insurmountable, but not a weekend project either.

(Just in case you don't have enough nightmares as it is, human cells do have OTHER suicide switches. With HIV, the ones in CD4+ T-helper lymphocytes are activated prematurely, and in NCI-H460 lung cancer, the tumorous cells STOP listening to commands to drop dead. More detail than you're likely to want in Wikipedia's article on apoptosis: [en.wikipedia.org] .)