With considerable variation including potential sex-specific differential rate of skeletal muscle loss, identifying modifiable factors for sarcopenia will be pivotal to guide targeted interventions. This study seeks to identify clinical and biological correlates of sarcopenia in community-dwelling older adults, with emphasis on the role of anabolic and catabolic stimuli, and special reference to gender specificity. In this crosssectional study involving 200 community-dwelling and functionally independent older adults aged ≥50 years, sarcopenia was defined using the Asian Working Group for Sarcopenia criteria. Comorbidities, cognitive and functional performance, physical activity and nutritional status were routinely assessed. Biochemical parameters included haematological indices, lipid panel, vitamin D level, anabolic hormones [insulin-like growth factor-1 (IGF-1), free testosterone (males only)] and catabolic markers [inflammatory markers (interleukin-6, Creactive protein) and myostatin]. Multiple logistic regression was performed to identify independent predictors for sarcopenia. Age was associated with sarcopenia in both genders. Malnutrition conferred significantly higher odds for sarcopenia in women (OR=5.71, 95 % CI 1.13-28.84.44, p=0.035) while higher but acceptable range serum triglyceride was protective in men (OR=0.05, 95 % CI 0.00-0.52, p=0.012). Higher serum myostatin independently associated with higher odds for sarcopenia in men (OR=1.11, 95 % CI 1.00-1.24, p=0.041). Serum IGF-1 was significantly lower amongst female sarcopenic subjects, with demonstrable trend for protective effect against sarcopenia in multiple regression models, such that each 1 ng/ml increase in IGF-1 was associated with 1 % decline in odds of sarcopenia in women (p=0.095). Our findings support differential pathophysiological mechanisms for sarcopenia that, if corroborated, may have clinical utility in guiding sex-specific targeted interventions for community-dwelling older adults.

BackgroundNonpharmacological interventions such as exercise and cognitive rehabilitation programs have shown promise in reducing the impact of dementia on the individual and the caregiver. In this study, we examine the effect of a multimodal cognitive and physical rehabilitation program for persons with mild dementia and their caregivers using conventional measures of cognition, behavior, quality of life (QoL), and caregiver burden together with goal attainment scaling (GAS), an individualized outcome measure.MethodsGoals were set at baseline, and GAS score was calculated at the end of the program. Participants were also assessed with the Chinese Mini-Mental State Examination, functional and behavioral scales (Barthel Index), Instrumental Activities of Daily Living, Neuropsychiatric Inventory Questionnaire, QoL, and caregiver burden using EuroQol-five dimension questionnaire and Zarit Burden Interview (ZBI). Differences in median scores postintervention were obtained. Further analysis of caregiver burden was undertaken utilizing the multidimensional classification of burden on the ZBI.ResultsThirty-four (61.8%) patients were assessed to have met their goals (GAS score≥50). Mean (standard deviation) GAS score was 48.6 (6.5). Cognition goals were set in only 20.6%, followed by goals to improve engagement and socialization; reduce caregiver stress; and improve physical function, behavior, and mood. Median scores in the cognitive, functional, and QoL measures did not differ significantly pre- and postintervention. The intervention had a positive impact on role strain, a unique dimension of caregiver burden.ConclusionThis study provides evidence that a multimodal approach combining physical exercise and cognitive rehabilitation improves goal attainment and caregiver burden in individuals and caregivers of persons with mild dementia.

A pro-inflammatory state exerts differential effects on physical frailty, contributing to the increased risk of baseline and progressive frailty only in the absence of a concomitant endocrine deficient state, with potential mediation via neurodegeneration.

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