There's a particular noncoding RNA that is found in the hypothalamus and declines sharply with age. Knock it out and you get shorter-lived, faster-aging mice with more senescence and fewer stem cells in the hypothalamus.
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How does this non-coding RNA (Hncsr) work? It binds a protein called YB-1, protecting it from degradation, and this protein inhibits the expression of the senescence marker p16. Not enough Hncsr and you impair the animal's ability to block senescence.
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A natural product found in black tea, Theaflavin 3-Gallate, was predicted by a virtual screen of molecules to mimic Hncsr's ability to protect YB-1, and indeed, administering it to middle-aged mice prevented hypothalamic stem cell senescence.
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The treated mice, after 6 months, also showed reduced age-related cognitive and motor deficits, better insulin sensitivity, and higher bone mass. The study didn't follow them long enough to test the effect on lifespan.
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Of course, this doesn't prove that this is the *only* mechanism causing hypothalamic stem cell decline or aging symptoms downstream of it. But it does show that this is *a* causal mechanism.
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You know how people make graphs of the expected lifespan of humans over time? Like we tend to live a couple of years longer this century than we did last century and so on. I'd like to see that for lab mice.
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Ask and thou shalt receive (Thread I did https://twitter.com/ArtirKel/status/1188522622998450176 … )
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