Researchers here uncover a set of characteristic molecular changes that correlate well with chronological and biological age. This is not the only such discovery in recent years: DNA methylation patterns are another candidate for biomarker of aging, and it may yet be the case that some form of telomere measurement might also do the job. It is important to have a good way to measure biological age, how damaged an individual is, as how else is the research community to effectively evaluate the first generation of prospective rejuvenation treatments when they arrive? The wait and see approach of life span studies is already far too expensive in time and money when carried out in laboratory mice, and certainly impractical in humans on an ongoing basis.
Fine structural details of glycans attached to the conserved N-glycosylation site significantly not only affect function of individual immunoglobulin G (IgG) molecules but also mediate inflammation at the systemic level.
By analyzing IgG glycosylation in 5,117 individuals from four European populations, we have revealed very complex patterns of changes in IgG glycosylation with age. Several IgG glycans (including FA2B, FA2G2, and FA2BG2) changed considerably with age and the combination of these three glycans can explain up to 58% of variance in chronological age, significantly more than other markers of biological age like telomere lengths. The remaining variance in these glycans strongly correlated with physiological parameters associated with biological age.
Thus, IgG glycosylation appears to be closely linked with both chronological and biological ages. Considering the important role of IgG glycans in inflammation, and because the observed changes with age promote inflammation, changes in IgG glycosylation also seem to represent a factor contributing to aging.