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S100A1 as a New Biomarker for Assessing Frailty in Elderly Patients with Heart Disease

S100A1 as a New Biomarker for Assessing Frailty in Elderly Patients with Heart Disease

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New research identifies the gene S100A1 as a potential biomarker for frailty in older patients with heart disease, paving the way for improved diagnosis and targeted therapies to maintain muscle health and mobility.

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Frailty, a condition marked by increased vulnerability and decline in physical capabilities, is becoming an increasingly important health concern among aging populations, especially those suffering from heart disease. Characterized by heightened risks of falls, hospitalization, postoperative complications, and general functional impairment, frailty demands better diagnostic and therapeutic approaches.

Recent research led by the German Institute of Human Nutrition Potsdam-Rehbruecke (DIfE), in collaboration with the University of Potsdam and the Deutsches Herzzentrum der Charité, has identified the gene S100A1 as a promising biomarker for frailty. This discovery stems from comprehensive gene expression studies performed on muscle tissue of older patients undergoing cardiac procedures such as surgery or transcatheter aortic valve implantation (TAVI). Involving 63 patients over 70 years of age, the study analyzed tissue samples from thigh muscles before interventions, assessing molecular changes associated with frailty phenotypes such as gait speed, grip strength, and mobility.

The team pinpointed ten genes with altered expression linked to frailty, with S100A1 standing out due to its crucial role in muscle function. Patients exhibiting lower S100A1 levels showed decreased muscle strength and impaired mobility, while higher blood levels of S100A1 correlated positively with better grip strength. Laboratory experiments confirmed that diminished S100A1 hampers muscle development, and animal models indicated that higher S100A1 levels are associated with increased muscle mass, further boosted by exercise.

Dr. Omar Baritello from the FGW explained, "For the first time, we have demonstrated a clear connection between reduced S100A1 expression and frailty phenotypes." Study director Dr. Heike Vogel emphasized the potential of S100A1 not only as a biomarker for early detection but also as a therapeutic target to maintain muscle health and prevent frailty. Future research aims to validate S100A1 measurement in clinical settings and explore interventions such as targeted training or pharmaceuticals to modulate its expression.

Overall, this pioneering work enhances understanding of age-related muscle deterioration and offers hope for strategies that can improve the quality of life and safety of elderly individuals. Early identification of frailty using S100A1 could lead to personalized treatments, ultimately helping older adults preserve mobility and independence. Source

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