Hacker News
Found: A protein that drives ageing without unleashing inflammation
neom
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Granzyme K is the protein.
ethanj8011
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> Despite persistent immune aging phenotypes, GzmK deficiency markedly attenuated organ aging, effectively uncoupling immune and tissue aging... These findings identify GzmK as a tissue-specific driver of organismal aging but not immune aging or systemic inflammaging.
StilesCrisis
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A_D_E_P_T
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> GzmK does not affect steady-state immune aging or aged immune responses after challenge
Virtually all old mice die of cancer, especially in the lab. If GzmK doesn't mitigate immune system aging, GzmK-null mice are still going to die of cancer, for little or no change in lifespan. (But presumably an improved healthspan due to reduced soft tissue and bone aging.)
hagbard_c
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Bret Weinstein did research on this topic which suggested that this is caused by lab mice having extraordinarily long telomeres which cause them to be good at cell repair but bad at limiting neoplasm growth due to delayed apoptosis. The result of this combination would be that lab tests on potential damage done by preparations on these mice is less valid 'cause they are better at repairing such damage than the average mammal due to those long telomeres. It also means nearly all these mice succumb to cancer. They're not normal mice, at all.
The reserve-capacity hypothesis: evolutionary origins and modern implications of the trade-off between tumor-suppression and tissue-repair
Bret S Weinstein 1 , Deborah Ciszek
therein
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Is this related to them being cloned? Did anyone try to get some random mice or is that too taboo?
cyberax
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This is a huge problem for medical research. Imagine that you conduct a safety test of your compound on mice, and 25% of the test group die of cancer within 1 year. That's bad, right? Well, the control group also has 20% cancer rate.