I don't expect them to be ready in time to immortalize anybody reading this, certainly not codgers like de Gray and Kurzweil. When my 5-year-old asks me what the world will be like in 100 years, I tell him we'll most likely all be dead. But it's theoretically possible.
You don't even need them to reduce glycosylation. There are drugs in development that reverse it. Here's one that looked promising, but the company ran out of money before they ran out of red tape:
http://en.wikipedia.org/wiki/Alagebrium
ISTR that there are supposedly better medications that do the same thing in the works.
Known crosslink breakers (e.g., alagebrium, of the thiazolium halide family) are only partly effective because they break only a subset of AGE crosslink structures (sugar-derived alpha-diketone bridges). So far, no agent has been found that breaks the prevalent glucosepane and K2P crosslink structures. Enzymes that would be able to recognize and disassemble glycation products may be too big to migrate into the ECM and repair collagen or elastin in vivo.
Meanwhile, over the next decade, glycation -- that might otherwise have been largely-inhibited by simple and inexpensive glycation-inhibition regimens -- will turn today's:
* 20-year-olds into further-degraded 30-year-olds,
* 30-year-olds into further-degraded 40-year-olds,
* 40-year-olds into further-degraded 50-year-olds,
* etc.
The point is that glycation is just a chemical reaction which can be reversed. You need to get something there which can reverse the chemical reaction. It's not necessarily easy, but it's not necessarily impossible either. There are also other potential ways to deal with A.G.Es, like stimulating turnover of those molecules, or, as you implied, preventing their formation.
I'm not trying to imply that todays n year olds won't be 2019's n+10 year olds, or 2050's fertilizer. I'm just saying it's possible in theory.
How does one cure glycation and mitochondrial decay? http://www.lef.org/magazine/mag2008/apr2008_Protecting-Again...