Researchers have in the past couple of years shown that GDF11 levels decline with age in mice, and that restoring youthful GDF11 in old mice improves numerous measures of health. The mechanism involved may be increased stem cell activity. There has been some debate over whether the teams involved are in fact measuring what they think they are measuring, however. New human data in the research noted here today muddies the water some more, though these researchers are also claiming an improvement in the approach to measurement of GDF11 levels. This suggests that either mice and humans are different in this aspect of aging, or that the issues in prior methods of measurement were more prevalent than thought, or both. The outcome of improved health in aged mice following introduction of additional GDF11 isn't disputed, so it will be interesting to see how these various results are reconciled:
Researchers have developed an accurate way to measure a circulating factor, called GDF11, to better understand its potential impact on the aging process. They found that GDF11 levels do not decline with chronological age, but are associated with signs of advanced biological age, including chronic disease, frailty and greater operative risk in older adults with cardiovascular disease. "Aging is the primary risk factor for the majority of chronic diseases, so it is critical to identify and understand the biomarkers, or indicators, in the body that are linked to this process. The role of GDF11 as a biomarker of aging and its association with age-related conditions has been largely contradictory, in part, because of how difficult it has been to measure. We have developed a new way to measure GDF11 that is accurate and effective."
A challenge of previous measurements was differentiating between the circulating levels of GDF11 and those of a highly-related protein, myostatin. To overcome this, researchers developed an extremely precise assay that can distinguish between unique amino acid sequence features, or "fingerprints" of GDF11 and myostatin. Using this platform, researchers compared age-associated changes in GDF11 and myostatin in healthy men and women between 20 and 94 years old. They discovered that although myostatin is higher in younger men than younger women and declines in healthy men throughout aging, GDF11 levels do not differ between sexes nor decline throughout aging. In an independent cohort of older individuals with severe aortic stenosis, researchers found that those with higher GDF11 levels were more likely to be frail and have diabetes or prior cardiac conditions. Following valve replacement surgery, increased GDF11 was associated with a higher prevalence of re-hospitalization and multiple adverse events.
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