

DNA Markers Distinguish Sarcopenia from Frailty
Sep 17, 2021
04:46
Sarcopenia is a common clinical condition that befalls the elderly—defined as a loss of skeletal muscle and muscle strength. Sarcopenic patients share clinical features with physical frailty (a subtype of the condition of frailty). Frailty is a broadly defined condition that typically encompasses multiple domains of aging, including cognitive impairment and decreased mobility and social activity. Sarcopenia and frailty are both deeply affected by aging, however, the underlying metabolic bases they stem from have remained unclear. How molecularly similar are sarcopenia and frailty? Are they spawned from the same cause?
“[…] little is known about the metabolic basis of sarcopenia, either shared with or discrete from frailty.”
In 2021, researchers from Kyoto University and Okinawa Institute of Science and Technology Graduate University collected blood samples from a cohort of elderly participants (from a previous study on frailty), and analyzed the samples in relation to sarcopenia. Their research paper was published as the cover of Aging (Aging-US) Volume 13, Issue 17, and entitled, “Reduced uremic metabolites are prominent feature of sarcopenia, distinct from antioxidative markers for frailty.”
Full blog - https://www.impactjournals.com/journals/blog/aging/trending-with-impact-metabolomics-discerns-sarcopenia-from-frailty/
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DOI - https://doi.org/10.18632/aging.203498
Full text - https://www.aging-us.com/article/203498/text
Correspondence to: Mitsuhiro Yanagida email: myanagid@gmail.com
Keywords: sarcopenia, muscle mass, metabolomics, frailty, uremic metabolites, aging
About Aging-US
Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.
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