As far as updates, prophets (the name here is so perfectly ironic), the guy who got downvoted for suggesting that the MoA for resveratrol is upstream of AMPK, seems to be correct, in that resveratrol's target might be PDE4 inhibition, and therefore probably works through cAMP, causing epac1 to release calcium causing a CaMKK dependent activation of AMPK. So aside from CREB mediated gene transcription of PGC-1alpha, the vast majority of resveratrol's activity seems to be working through AMPK. prophets was just wrong in suggesting it was LKB1 instead of CaMKK controlling the AMPK activity.
All of that is not to belittle geddarkstorm's theory, dude (or dudette) was talking about some cutting edge stuff for the time. It's 5 years later, and everyone's hyped on NAD+ precursors and nobody knows about activating NAMPT. Basically 5 years ago he was ahead of most people now.
NAMPT still seems to be a very valid target for increasing healthspan and possibly even lifespan, IMO AMPK even looks more promising through its ability to regulate NAMPT as well as a variety of other important factors (PGC1alpha, FOX proteins, inhibition of mTOR's downstream targets etc.)
AMPK is the under-appreciated sister of the sirtuins, each are essential for the full functionality of the other, and I've always scratched my head as to why the sirtuins get all the limelight when AMPK is an equally valuable therapy target.
P.S. Ive thought about bumping this thread myself due to all the nicotinamide riboside and NMN hype. NAMPT activators are the perfect replacement for these overpriced NAD+ precursors.
Edited by Bateau, 17 November 2014 - 12:10 AM.
