skip to Main Content

Radiocarbon dating reveals minimal collagen turnover in both healthy and osteoarthritic human cartilage.

Here, these researchers evaluated collagen turnover in the cartilage of 23 individuals born between 1935 and 1997, whom did (15 people) or didn't (8 people) have osteoarthritis. They report that " virtually no replacement of the collagen matrix happened after skeletal maturity...in tibial plateau cartilage...and that neither osteoarthritis nor tissue damage influenced collagen turnover ." I suspect this may influence how we might think of AGE accumulation in cartilage, so I have tagged it appropriately.
Read More

The effect of 1 year of Alagebrium and moderate-intensity exercise training on left ventricular function during exercise in seniors: a randomized controlled trial.

Here, these researchers test whether alagebrium, known to affect advanced glycation endproducts (AGEs), would be any more effective at reducing age-related cardiovascular stiffening if it is paired with regular, moderate-intensity exercise for 1 year. They found that even with alagebrium with 1 year of this exercise, some measures (stroke index and effective arterial elastance) were still below those of lifelong exercising controls, suggesting that alagebrium may not have remarkable positive effects on cardiovascular elasticity in human aging.
Read More

Enhanced external counterpulsation (EECP) decreases advanced glycation end products and proinflammatory cytokines in patients with non-insulin-dependent type II diabetes mellitus for up to 6 months following treatment.

I did not yet look at the full-text to determine which "AGEs" were measured; I assume it was albumin or something else turned over relatively quickly. But that these "AGEs" were decreased by 75% at 48 hours after treatment is remarkable; I wonder what's going on here. Note: external counterpulsation is a mechanical, non-invasive intervention whereby pressure is applied to the vasculature in a certain rhythm with the heart beat. It is apparently sometimes used to treat angina, and is suspected to theoretically enhance angiogenesis due to shear stresses caused by the technique (see https://my.clevelandclinic.org/health/articles/eecp ). The question of why these reductions in AGEs are so large, happen so quickly, and persist so long in response to this technique, is fascinating to me, and I suspect will be for others on this list. I wonder what AGE-relevant proteins, enzymes, and systems are activated or enhanced by this technique.
Read More

Effect of aging and exercise on the tendon.

The authors of this review of tendon biology in response to aging and exercise note that "turnover of the core of the tendon after maturity is very slow or absent...while glycation-derived cross-links increase substantially". I wonder what the relevance might be, of their statement: "it seems that resistance training can yield increased stiffness and modulus of the tendon and may reduce the amount of glycation." If so, I wonder what the mechanism is, and the species of AGEs that might be reduced with resistance training.
Read More

Identification of C1q as a Binding Protein for Advanced Glycation End Products.

A few years ago I reported on C1q "dramatically increasing in the CNS during normal aging" (PMID 23946404). I retained this one to illustrate a connection between C1q and AGEs. The authors of the current report note that "the binding specificity of C1q might be ascribed, at least in part, to the electronegative potential of the ligand proteins". I wonder if the current report might help explain why "C1q dramatically increases in the CNS during normal aging", and that this dramatic increase may not be a type of "accumulating, stable, age-related damage" needing "cleaned" up SENSibly.
Read More

Protein carbamylation is a hallmark of aging.

Here, these authors contrast carbamylation with glycation, and assert that perhaps carbamylation is also a (more?) relevant and/or important, persistent, accumulating protein modification with aging. They also suggest the possibility of carbamylation repair/cleanup enzymes (perhaps similar in function to glyoxalase enzymes) which may decline in aging, contributing to (or causing) this observed accumulation of carbamylation-derived products (CDPs).
Read More

Skin collagen advanced glycation endproducts (AGEs) and the long-term progression of sub-clinical cardiovascular disease in type 1 diabetes.

I rarely see papers that measure and report on glucosepane in humans, so I wanted to report this paper, even though it was in type 1 diabetics. Here, the authors (including Vincent Monnier) report that in these type 1 diabetics, glucosepane, pentosidine, and the methylgyoxal hydroimidazolones ("MG-H1") correlated with intima-media thickness change from year 1 to 6, while left ventricular mass (a potential proxy of arterial stiffness) also correlated with MG-H1. While I'm not confident that type 1 diabetics are a good model for human cardiac aging and AGE deposition, I suspect some on this list will want to read this report.
Read More

Free report on high blood pressure

The American Heart Association estimates more than 100 million Americans have high blood pressure, also known as “hypertension”. Learn more about the cause of high blood pressure and how you can reverse it in our free report.

Coming soon. We’ll send you the report as soon as it’s published.

*We do not share your email address with anyone.

Free longevity biomarker report

Biomarker levels predict the risk of early death—and we can change them! Learn about some important longevity biomarkers in our free report.

Coming soon. We’ll send you the report as soon as it’s published.

*We do not share your email address with anyone.

Free diabetes report

An estimated 50% of American adults have either prediabetes or type 2 diabetes. Learn more about the cause of type 2 diabetes, prediabetes, insulin resistance, and how to reverse them in our free report.

Coming soon. We’ll send you the report as soon as it’s published.

*We do not share your email address with anyone.

Back To Top