[spangry]

Yeah I oversimplified protein 'chaperoning' for brevity's sake. As for prion recruitment of other proteins leading to amyloid plaque formation in the brain, I concede it's an open question. But my money would be on 'yes' to this hypotheses, given recent studies that have been coming out (except for a particular German one that concluded the opposite based on a mouse model of PD).

I'm probably on the wrong end of the metabolic semantics here; I was specifically referring to hydrolysis (or is the correct term hydrogenation?) occurring in red-blood cells. If this is not considered part of normal metabolic processed then mea culpa. The particular (pro)drug I mentioned (likely) relies on this mechanism to cleave/dissolve a covalent bond between the two constituents of the prodrug, to produce a 'time-release' effect: the constituents being l-lysine and dexamfetamine/dextroamphetamine ('lisdexamfetamine').

For example, here's one of the few serious studies I've been able to find on its metabolism (i.e. not a single dose study that concludes 'yes, this leads to amphetamine in the blood'): http://www.tandfonline.com/doi/full/10.3109/21556660.2013.77... . There was another (better) one somewhere on pubmed, but I can't seem to find it atm (although it was also an in vitro study). I also found this, more general paper, quite interesting (although I'm guessing it's outdated?): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1142344/

I admit, my understanding of the process by which amino-acids are synthesised in to proteins in vivo is not the best. I'm actually a little hazy on how I first arrived at the notion that an over-abundance of l-lysine could disrupt the Krebs-cycle. I probably came up with it during one of my long treks across Wikipedia, so it's very likely wrong....