IgG glycome profiles in 20,405 people linked to biological aging and mortality risk
In an abstract analyzing IgG glycome composition in 20,405 people from 42 studies, specific glycan profiles reflected accelerated biological aging and were strongly associated with higher all-cause mortality risk, independent of established risk factors; this is an association, not proof of cause. [1]
Automatic summary · not editorially reviewed
The key findings
IgG glycome composition was analyzed in 20,405 individuals from 42 studies processed at one laboratory between 2008 and 2025. [1]
Accelerated glycan aging was strongly associated with increased all-cause mortality risk, independent of established risk factors and potential confounders. [1]
The authors propose IgG glycans as a possible functional link between chronic inflammation, aging, disease susceptibility and all-cause mortality. [1]
The source at a glance
- Study type / format
- Abstract of an analysis of IgG glycome composition across 42 studies
- Population / context
- 20,405 individuals from 42 different studies
- Summary based on
- Study abstract
- Publication status
- Preprint · peer-review status not confirmed
- Original publication
- April 23, 2026
IgG glycans measured in 20,405 people across 42 studies
The abstract describes IgG glycosylation as a structural modification that modulates antibody effector functions and helps balance inflammation. Altered IgG glycosylation has been reported in many diseases, often years before clinical manifestation, which the authors say suggests a possible causal role and biomarker potential. The analysis covered IgG glycome composition in 20,405 individuals from 42 different studies, all processed at the Genos Glycoscience Research Laboratory between 2008 and 2025.
Supporting source [1]
Accelerated glycan aging and all-cause mortality risk
Across nearly all diseases, specific IgG glycome profiles reflected accelerated biological aging, according to the abstract. Accelerated glycan aging was strongly associated with increased risk of all-cause mortality, independent of established clinical risk factors and potential confounders. The abstract also reports that interventions known to reduce mortality risk — hormone replacement therapy, therapeutic plasma exchange and caloric restriction — were associated with reversal of glycan aging. These are associations; the abstract does not show that changing glycans causes changes in mortality.
Supporting source [1]
Proposed inflammation link remains untested in this abstract
The authors suggest that, given their role in modulating low-grade systemic inflammation, IgG glycans may represent a functional link between chronic inflammation, aging, disease susceptibility and all-cause mortality. This is a proposed interpretation, not a demonstrated mechanism. The abstract does not report study designs, follow-up durations, how biological age was measured, or effect sizes, and the full text was not reviewed.
Supporting source [1]
How to interpret this
Abstract only; the full text was not reviewed. Study designs, follow-up, how biological age was measured and effect sizes are not reported. Associations do not establish causation, and the inflammation link is proposed, not demonstrated.
Based on the study abstract; the full paper, tables and supplementary data were not reviewed.
Source & supporting passages
Mijakovac A, Butz E, Vučković F, Hodžić AF, Rapčan B, Kifer D, Deriš H, Trbojević BR, Lukšić F, Cindrić A, Gudelj I, Briški NŠ, Josipović G, Yuksel ZS, Ćatić J, Šaler F, Szavits-Nossan J, Hedin CRH, Šimunović J, Borošak I, Krištić J, Monteiro-Martins S, Pribić T, Hanić M, Pučić-Baković M, Trbojević-Akmačić I, Štambuk T, Štambuk J, Kavur MM, Fančović M, Cvetko A, Pezer M, Polašek O, Gornik O, Kiprov D, Verdin E, Younggren B, Newson L, Menni C, Steves CJ, Spector TD, Halfvarson J, Pocheć E, Szewczyk M, Turkalj M, Wilson JF, Alarcon-Riquelme ME, Aden K, Rosenstiel P, Franke A, Frey N, Schreiber S, Blaak EE, Köttgen A, Zoldoš V, Primorac D, Marjanović D, Schultheiss UT, Wang W, Lauc G. · europepmc.org · April 23, 2026