Glucosepane Culprit Options

[KoolK3n]

Glucosepane is currently considered to be the most important cross-linking AGE yet discovered because its levels are found to be 10 to 1000 times higher in human tissue than any other cross-linking AGE.

http://en.wikipedia.org/wiki/Glucosepane

[Jakare]

Glucosepane is currently considered to be the most important cross-linking AGE yet discovered because its levels are found to be 10 to 1000 times higher in human tissue than any other cross-linking AGE.

http://en.wikipedia.org/wiki/Glucosepane

I wonder if there is someone trying l-carnosine to remove it (Pubmed doesn´t show any results) Would make more sense to help the body to keep its ability to get rid of it as the present AGEs inhibitors don´t affect much the aging process although useful for some conditions.

[Jakare]

http://www.longecity.org/forum/topic/55512...teins-in-aging/

[KoolK3n]

I wonder if there is someone trying l-carnosine to remove it (Pubmed doesn´t show any results) Would make more sense to help the body to keep its ability to get rid of it as the present AGEs inhibitors don´t affect much the aging process although useful for some conditions.

Yes, helping the body would also help minimize AGEs such as reducing sugar consumption. Increasing insulin resistance aggravates certain AGEs. Even if commercial AGE inhibitors have little effect on AGE, wouldn't it still be worth it? Limited research suggests these are cheap options to reduce some AGE crosslinks:
http://en.wikipedia.org/wiki/Advanced_glyc...c_interventions

http://www.ncbi.nlm.nih.gov/pubmed/16706655
No promises but inspiring. Though, I do not understand what "ECM turnover enhancement" means..

α-Dicarbonyl trap (aminoguanidine) seems to have to many side-effects:
http://en.wikipedia.org/wiki/Aminoguanidine

The two Thiazolium salts on this Wikipedia page are not entirely accurate:
http://en.wikipedia.org/wiki/Glucosepane#Thiazolium_salts

Here's why:
-Any sort of ALT-711 production is currently absent
-PTB (N-phenacylthiazolium bromide) http://www.ncbi.nlm.nih.gov/pubmed/11520302

The prospects absolutely warrant further research based on what I'm finding.

[Jakare]

Alagebrium is an AGE-breaker, a compound that dissolves some forms of advanced glycation end-products (AGEs), compounds implicated in the damage of aging. Unfortunately, the specific types of AGEs affected by alagebrium, also known as ALT-711, are more important in rats than humans.

http://www.fightaging.org/archives/2009/02...-alagebrium.php

As you said further research focused in Glucosepane is needed. In the meantime a healthy diet, Benfotiamine and L-Carnosine seem to be the best options for AGEs 'partial' prevention.

Though, I do not understand what "ECM turnover enhancement" means..

I think it means that as cross-linking occurs the ECM Extracellular Matrix becomes less permeable and so then less prone to be cleansed. 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 So by talking of the enhancement of ECM turnover they seek to make the matrix permeable enough for the enzymes to tresspass and degrade the damaged protein, which will be replaced. As they said that wouldn´t be the perfect solution and is kind of a delicate process.

[KoolK3n]

I think it means that as cross-linking occurs the ECM Extracellular Matrix becomes less permeable and so then less prone to be cleansed. 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 So by talking of the enhancement of ECM turnover they seek to make the matrix permeable enough for the enzymes to tresspass and degrade the damaged protein, which will be replaced. As they said that wouldn´t be the perfect solution and is kind of a delicate process.

Thanks! What's the method for enhancement? Google brings up very little results.

[KoolK3n]

http://www.longecity.org/forum/topic/55512...teins-in-aging/

Just finished watching it. It led me to this: http://en.wikipedia.org/wiki/NFE2L2#Nrf2_as_a_drug_target
Then this: http://en.wikipedia.org/wiki/Bardoxolone_methyl#Phase_2 (Second paragraph)
Wouldn't oral creatine supplementation counteract the problem? Assuming exercise triggers the phosphorylation of creatine and yada yada yada donates a phosphate group to ADP to form ATP.

Another question, why are many of these clinical drugs targeted for specific conditions? For example, if RTA-402 increases Nrf2 transcription. Wouldn't it overwhelmingly have more potential than just for advanced chronic kidney disease type-2 diabetes mellitus patients? Wouldn't anyone aging benefit from Nrf2 amplification?