In the context of accelerated aging of the population worldwide, frailty has emerged as one of the main risk factors that can lead to loss of self-sufficiency in older people. This syndrome is defined as a reduced state of physiological reserve and functional capacity. The main diagnostic tools for frailty are based on scales that show deficits compared to their clinical application, such as the Fried frailty phenotype, among others. In this context, it is important to have one or more biomarkers with clinical applicability that can objectively and precisely determine the degree or risk of frailty in older people. The objective of this review was to analyze the biomarkers associated with frailty, classified according to the pathophysiological components of this syndrome (inflammation, coagulation, antioxidants, and liver function, among others). The evidence demonstrates that biomarkers associated with inflammation, oxidative stress, skeletal/cardiac muscle function, and platelet function represent the most promising markers of frailty due to their pathophysiological association with this syndrome. To a lesser extent but with the possibility of greater innovation, biomarkers associated with growth factors, vitamins, amino acids, and miRNAs represent alternatives as markers of this geriatric syndrome. Likewise, the incorporation of artificial intelligence represents an interesting approach to strengthening the diagnosis of frailty by biomarkers.

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Background: Frailty has emerged as one of the main geriatric syndromes to be prevented in order to improve quality of health and life in the elderly. In this sense, the characterization of this syndrome through reliable and feasible diagnostic tools for clinical use, such as the Frail Trait Scale 5 (FTS-5) and Frail Trait Scale 3 (FTS-3), represents the basis for this objective. Objectives: To characterize the frailty syndrome in a population of older adults using FTS-5, FTS-3, and Fried phenotype (FP) as frailty diagnostic tools. Design: Cross-sectional study. Participants: 300 adults ≥65 years recruited from different Family Health Centers and community groups of older people in Talca, Chile. Methods: The diagnosis of frailty was made according to FP, FTS-5, and FTS-3 tools. Data about sociodemographic characteristics and anthropometric measurements were collected by a clinical interview by a previously trained health professional. Results: A total prevalence of frailty according to the FP of 19.7% was observed; while in the group of women and men it was 21.4% and 15.0%, respectively. Concerning the FTS-5 tool, the total prevalence of frailty was 18%, while in the group of women and men was 18.0% and 17.5%, respectively. The FTS-3 tool shows a total prevalence of frailty of 23.3%, while in the group of women and men a prevalence of 22.7% and 25.0%, respectively. A significant difference is observed with respect to the presence of the Fried criteria of “weakness” (women: 21.4%, men: 38.8%) and “weight loss” (women: 16.8%, men: 7.5%; p < 0.05). A significant difference is observed concerning the average score of “Handgrip” criteria, “walking time”, and “Physical Activity Scale for the Elderly” (PASE) between the group of women and men. Frailty, diagnosed by FTS-3, is significantly associated with the risk factors of overweight (body mass index ≥ 25) (OR: 10.225, 95% CI: 1.297–80.617) and advanced age (age ≥ 75 years) (OR: 1.839, 95% CI: 1.040–3.250). Conclusion: The prevalence of frailty observed with the FTS-5 (18%) and FTS-3 (23.3%) tools are similar to the prevalence observed through the FP (19.7%) and those reported in other observational studies. Considering the similar prevalence of frailty diagnosed with the three tools, FTS-3 should be a valuable tool for the screening of frailty in the community.

Although platelets are anucleated cells, they have fully functional mitochondria, and currently, it is known that several processes that occur in the platelet require the action of mitochondria. There are plenty of mitochondrial-targeted compounds described in the literature related to cancer, however, only a small number of studies have approached their interaction with platelet mitochondria and/or their effects on platelet activity. Recent studies have shown that magnolia extract and mitochondria-targeted magnolol can inhibit mitochondrial respiration and cell proliferation in melanoma and oral cancer cells, respectively, and they can also induce ROS and mitophagy. In this study, the effect of triphenylphosphonium cation, linked by alkyl chains of different lengths, to the organic compound magnolol on human-washed platelets was evaluated. We demonstrated that the addition of triphenylphosphonium by a four-carbon linker to magnolol (MGN4) considerably enhanced the Magnolol antiplatelet effect by a 3-fold decrease in the IC50. Additionally, platelets exposed to MGN4 5 µM showed several differences from the control including increased basal respiration, collagen-induced respiration, ATP-independent respiration, and reduced ATP-dependent respiration and non-mitochondrial respiration.