If you had the perfect bioinformatics database + genomically-obsessed autist, it would be easier to deal with larger quantities of genes. Like, the human genome has 20k genes, and let’s say 1% are super-relevant for aging or brain preservation—that would be 2k genes, and that would be super-easy for an autistically-obsessed person to manage
I mean, sure, if we had a really fast car we could drive from New York to Orlando by going through Seattle. But (a) we don’t have that amazing database, and (b) it’s probably easier to be more efficient than to build the perfect bioinformatics database. With a focus on very-slow-turnover factors, the problem is unlikely to involve even 200 genes, let alone 2k.
You personally might very well be able to identify the full list of root causes, to a reasonably-high degree of certainty, without any tools beyond what you have now, by being more strategic—focusing effort on exactly the questions which matter.
If you had the perfect bioinformatics database + genomically-obsessed autist, it would be easier to deal with larger quantities of genes. Like, the human genome has 20k genes, and let’s say 1% are super-relevant for aging or brain preservation—that would be 2k genes, and that would be super-easy for an autistically-obsessed person to manage
Alternatively, aging (like most non-discrete phenotypes) may be omnigenic.
I mean, sure, if we had a really fast car we could drive from New York to Orlando by going through Seattle. But (a) we don’t have that amazing database, and (b) it’s probably easier to be more efficient than to build the perfect bioinformatics database. With a focus on very-slow-turnover factors, the problem is unlikely to involve even 200 genes, let alone 2k.
You personally might very well be able to identify the full list of root causes, to a reasonably-high degree of certainty, without any tools beyond what you have now, by being more strategic—focusing effort on exactly the questions which matter.
https://www.pnas.org/content/116/44/22173