There’s almost no intersection between papers so far — even the ones that refer to the same tissue type in the same species. Am I missing something, or is this fairly damning to the hypothesis “correlational signatures of aging & longevity make good drug targets”?
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By contrast, we do know a cluster of genes which, when knocked out, reliably extend life & prevent some age-related dysfunctions in multiple model organisms, namely the insulin/IGF/GH pathway.
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Of course, it would be prohibitively expensive to knock out every possible gene in a mouse and see if it lives longer. So we understandably don’t have many of these examples validated for lifespan in mammals. (There are more examples of “knockout rescues disease model.”)
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Maybe the problem with the transcriptomics is study design? N=16 biopsies, list all genes with p<0.05 difference between old & young transcript levels, is pretty typical, and maybe that’s just too much noise?
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Ok, not “maybe”, it is too much noise. I’ll add sample sizes, p-values, and relative fold changes to my notes; will write up results in a blog post.
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