Ages

Acronym for "Advanced Glycation Endproducts".

With endogenous glycation in the organism, as with exogenous glycation) sugar molecules (especially fructose, galactose and glucose) react with the body's own proteins without catalytic enzyme involvement. During this chemical reaction, bioactive molecules (e.g. dicarbonyls such as 3-deoxyglucosone and methylglyoxal) are formed as AEGs, which are progressively deposited and accumulate in the tissue with increasing age. The concentration of AGEs depends on the sugar supply. Endogenous AGE formation is enhanced by oxidative stress and chronic inflammation. AGEs are considered a strong independent predictive factor for arteriosclerosis, especially in diabetics and haemydialysis patients.

Among the diagnostically important AGEs is HbA1, which is formed during the glycation of hemoglobin and whose concentration plays an important diagnostic role in assessing average blood glucose levels.

Some AGEs promote inflammatory processes, partly by binding to a cellular receptor "Receptor for AGE (RAGE)" on monocytes. In neurons, glycation can lead to degenerative degradation of myelin and neuropathies. This process plays a role in diabetes mellitus type II and Alzheimer's disease.

1. Makrantonaki E et al (2016) Skin ageing. Dermatologist 67: 730-737
2. Uribarri J et al(2007): Circulating glycotoxins and dietary advanced glycation endproducts: two links to inflammatory response, oxidative stress, and aging. J Gerontol A Biol Sci Med Sci 62: 427-433.