Comparison of Habitual and Maximal Gait Speed and their Impact on Sarcopenia Quantification in German Nursing Home Residents.

OBJECTIVES Sarcopenia is characterized by loss of muscle strength and muscle mass. The EWGSOP2 specifications include physical functioning determination for quantification of the sarcopenia severity. However, there is a lack in the use of habitual and maximal gait speed and their influence on sarcopenia quantification. We hypothesize differences in sarcopenia quantification using habitual and maximal gait speed. METHODS Sixty-six residents from five nursing homes were examined. Habitual and maximal gait speed were measured by 4-meter-walking-Test. McNemar-Test and χ2-test were used to identify quantification differences. Effect sizes of both gait speeds were calculated with Spearman's rank-correlation-coefficient. RESULTS Significant difference was identified for twenty-two residents in physical functioning classification by McNemar-Test (p<.001). χ2-Test identified a significant frequency distribution for sarcopenia categories between both gait speeds (χ2 (df2)=11.215, p=.004; Cramer's V=.412). Significant correlations (p<.05) were only shown for maximal gait speed in variables falls in the last three months (|rs|=.326), Barthel-Index (|rs|=.415), and SARC-F (|rs|=.335). CONCLUSIONS The use of habitual and maximal gait speed has a significant impact on sarcopenia quantification in nursing home residents. An adapted standardization in the EWGSOP2 specifications should follow

Feasibility of a Geriatric Assessment to Detect and Quantify Sarcopenia and Physical Functioning in German Nursing Home Residents-A Pilot Study.

BACKGROUND Entering into a nursing home leads to increased immobility and further reductions in physical and cognitive functioning. As a result, there is a risk of sarcopenia, which is characterized by loss of muscle strength, muscle mass and physical functioning. To our knowledge, the feasibility of sarcopenia screening has not yet been performed in the German nursing home setting. METHODS For sarcopenia screening, the specifications of EWGSOP2 were applied. The quantification of sarcopenia was performed according to the corresponding cut-off values. The collection of anthropometric data and the morbidity status were recorded. SARC-F, mini-mental state examination, Barthel Index, Short Physical Performance Battery and Timed Up and Go tests were implemented. RESULTS In one participant, severe sarcopenia could be identified. The quantification was not possible for four participants. A suspicion of sarcopenia was not confirmed in five participants. Only one person was able to perform all assessments. CONCLUSIONS Sarcopenia screening according to EWGSOP2 presented satisfactory feasibility by nursing home residents. However, further tests to assess the physical functioning of the participants often could not be performed. Moreover, inconsistencies in individual assessments became apparent, leading to inconclusive analyses. The recording of sarcopenia prevalence in German nursing homes should be the goal of further research

Microfluidic Chemotaxis Platform for Differentiating the Roles of Soluble and Bound Amyloid-β on Microglial Accumulation

Progressive microglial accumulation at amyloid-β (Aβ) plaques is a well-established signature of the pathology of Alzheimer's disease, but how and why microglia accumulate in the vicinity of Aβ plaques is unknown. To understand the distinct roles of Aβ on microglial accumulation, we quantified microglial responses to week-long lasting gradients of soluble Aβ and patterns of surface-bound Aβ in microfluidic chemotaxis platforms. We found that human microglia chemotaxis in gradients of soluble Aβ42 was most effective at two distinct concentrations of 23 pg.mL−1 and 23 ng.mL−1 Aβ42 in monomers and oligomers. We uncovered that while the chemotaxis at higher Aβ concentrations was exclusively due to Aβ gradients, chemotaxis at lower concentrations was enhanced by Aβ-induced microglial production of MCP-1. Microglial migration was inhibited by surface-bound Aβ42 in oligomers and fibrils above 45 pg.mm−2. Better understanding of microglial migration can provide insights into the pathophysiology of senile plaques in AD

A Low Dose of Dietary Resveratrol Partially Mimics Caloric Restriction and Retards Aging Parameters in Mice

Resveratrol in high doses has been shown to extend lifespan in some studies in invertebrates and to prevent early mortality in mice fed a high-fat diet. We fed mice from middle age (14-months) to old age (30-months) either a control diet, a low dose of resveratrol (4.9 mg kg−1 day−1), or a calorie restricted (CR) diet and examined genome-wide transcriptional profiles. We report a striking transcriptional overlap of CR and resveratrol in heart, skeletal muscle and brain. Both dietary interventions inhibit gene expression profiles associated with cardiac and skeletal muscle aging, and prevent age-related cardiac dysfunction. Dietary resveratrol also mimics the effects of CR in insulin mediated glucose uptake in muscle. Gene expression profiling suggests that both CR and resveratrol may retard some aspects of aging through alterations in chromatin structure and transcription. Resveratrol, at doses that can be readily achieved in humans, fulfills the definition of a dietary compound that mimics some aspects of CR

Sirt3, Mitochondrial ROS, Ageing, and Carcinogenesis

One fundamental observation in cancer etiology is that the rate of malignancies in any mammalian population increases exponentially as a function of age, suggesting a mechanistic link between the cellular processes governing longevity and carcinogenesis. In addition, it is well established that aberrations in mitochondrial metabolism, as measured by increased reactive oxygen species (ROS), are observed in both aging and cancer. In this regard, genes that impact upon longevity have recently been characterized in S. cerevisiae and C. elegans, and the human homologs include the Sirtuin family of protein deacetylases. Interestingly, three of the seven sirtuin proteins are localized into the mitochondria suggesting a connection between the mitochondrial sirtuins, the free radical theory of aging, and carcinogenesis. Based on these results it has been hypothesized that Sirt3 functions as a mitochondrial fidelity protein whose function governs both aging and carcinogenesis by modulating ROS metabolism. Sirt3 has also now been identified as a genomically expressed, mitochondrial localized tumor suppressor and this review will outline potential relationships between mitochondrial ROS/superoxide levels, aging, and cell phenotypes permissive for estrogen and progesterone receptor positive breast carcinogenesis

SIRT1 contributes to telomere maintenance and augments global homologous recombination

SIRT1 is a positive regulator of telomere length and attenuates age-associated telomere shortening

Epigenetic regulation of caloric restriction in aging

The molecular mechanisms of aging are the subject of much research and have facilitated potential interventions to delay aging and aging-related degenerative diseases in humans. The aging process is frequently affected by environmental factors, and caloric restriction is by far the most effective and established environmental manipulation for extending lifespan in various animal models. However, the precise mechanisms by which caloric restriction affects lifespan are still not clear. Epigenetic mechanisms have recently been recognized as major contributors to nutrition-related longevity and aging control. Two primary epigenetic codes, DNA methylation and histone modification, are believed to dynamically influence chromatin structure, resulting in expression changes of relevant genes. In this review, we assess the current advances in epigenetic regulation in response to caloric restriction and how this affects cellular senescence, aging and potential extension of a healthy lifespan in humans. Enhanced understanding of the important role of epigenetics in the control of the aging process through caloric restriction may lead to clinical advances in the prevention and therapy of human aging-associated diseases

Identification of Sarcopenic Obesity in German Nursing Home Residents—The Role of Body Composition and Malnutrition in the BaSAlt Cohort-Study

Background: Sarcopenic obesity (SO) is a phenotype, which is defined by reduced muscle strength, muscle mass, and obesity. Limited mobility leads to increased sedentary behavior and decreased physical activity. Both sarcopenia and obesity are aggravated by these factors. In combination, SO is an additional challenge for the setting nursing home (NH). Previous studies have shown a low prevalence of residents with SO in comparable settings, such as community-dwelling. We hypothesize that the BaSAlt cohort also has a small proportion of residents with SO. Methods: For the analysis, 66 residents (women: 74.2%) aged ≥ 65 years from NH, were screened for SO based on EWGSOP2 specifications and cut-off values to classify obesity. Results: Severe sarcopenia was quantified in eleven residents (16.7%). The majority of sarcopenic residents were women (n = 10) compared to men (n = 1). However, no SO could be identified by assessment of body mass index, fat mass in percentage, and fat mass index. Conclusion: As expected, the setting-specific cohort showed a low number of SO. Furthermore, no case of SO was identified in our study. Sarcopenia was associated with an increased fat-free mass in NH residents. Nevertheless, sarcopenia and obesity play important roles in the preservation of residents’ health

Identification of Sarcopenic Obesity in German Nursing Home Residents-The Role of Body Composition and Malnutrition in the BaSAlt Cohort-Study.

BACKGROUND Sarcopenic obesity (SO) is a phenotype, which is defined by reduced muscle strength, muscle mass, and obesity. Limited mobility leads to increased sedentary behavior and decreased physical activity. Both sarcopenia and obesity are aggravated by these factors. In combination, SO is an additional challenge for the setting nursing home (NH). Previous studies have shown a low prevalence of residents with SO in comparable settings, such as community-dwelling. We hypothesize that the BaSAlt cohort also has a small proportion of residents with SO. METHODS For the analysis, 66 residents (women: 74.2%) aged ≥ 65 years from NH, were screened for SO based on EWGSOP2 specifications and cut-off values to classify obesity. RESULTS Severe sarcopenia was quantified in eleven residents (16.7%). The majority of sarcopenic residents were women (n = 10) compared to men (n = 1). However, no SO could be identified by assessment of body mass index, fat mass in percentage, and fat mass index. CONCLUSION As expected, the setting-specific cohort showed a low number of SO. Furthermore, no case of SO was identified in our study. Sarcopenia was associated with an increased fat-free mass in NH residents. Nevertheless, sarcopenia and obesity play important roles in the preservation of residents' health