Hi everyone, today I wanted to share a video to speak about GlycanAge and inflammaging:
This is my first ever video… so please be cool with me especially with my french accent
but dot hesitate of course to tell me what do you think about it ![]()
My hypothesis here is that ManNac is not only a precursor of sialic acid (and a safe one unlike udp galactose…)
In this study ManNAc protects against podocyte pyroptosis via inhibiting mitochondrial damage and ROS/NLRP3 signaling pathway in diabetic kidney injury model - PubMed we can see for instance that in a diabetic kidney injury model, that ManNAc protected podocytes by inhibiting mitochondrial damage and the ROS/NLRP3 pyroptosis pathway. This is not GlycanAge evidence, but it supports a possible anti-inflammatory mechanism. So also would help the center part (part 2) I speak in my video (improve galactosylation > increase G2/G0)
A 2025 antibody glycoengineering study reported that ManNAc reduced Man5 high-mannose glycoform abundance through a gne mediated metabolic channeling mechanism involving UDP-n acetyl glucosamine and CMP-Neu5Ac. Man5 is upstream of mature complex N-glycans, so this suggests ManNAc may influence more than just terminal sialylation.
And this study:
Is one of the most relevant human studies on ManNAc : an open-label phase 2 trial in patients with GNE myopathy. GNE myopathy is a genetic disease caused by impaired biosynthesis of Neu5Ac. The trial included 12 patients and used oral ManNAc, 6 g twice daily, or 12 g/day.
The key result is that ManNAc increased plasma Neu5Ac and improved sarcolemmal sialylation after 90 days. The study also reported increased intracellular CMP-Neu5Ac.
Another interesting preclinical study showed that chronic oral ManNAc improved age asociated impairment of hippocampal synaptic transmission and long-term potentiation in senescence accelerated mice. This does not address GlycanAge or IgG glycosylation directly… but it supports the idea that ManNAc may have broader biological effects in aging models
Let me know yout thoughts and thanks for your support for thoses who liked the content ![]()
Cheers