Association between sarcopenia and depressive mood in urban-dwelling older adults: A cross-sectional study.

AIM: The aim of the present study was to examine the relationship between depressive mood and diagnostic components of sarcopenia. METHODS: The study used baseline data of participants in the Toyota Prevention Intervention for Cognitive Decline and Sarcopenia study. Participants in this cross-sectional study were 432 older adults (46.5% women, mean age 72.5 ± 4.7 years). We defined sarcopenia using the diagnostic algorithm recommended by the Asian Working Group for Sarcopenia, and all participants were classified into a sarcopenia or healthy control group. The skeletal muscle mass was measured by bioelectrical impedance. Depressive mood was assessed using the Geriatric Depression Scale-15 (range 0-15). RESULTS: Among the 432 participants, 9.5% were classified as having sarcopenia. The mean ± SD Geriatric Depression Scale-15 scores in the control and sarcopenia groups were significantly different at 3.9 ± 2.8 and 5.3 ± 3.3, respectively (P = 0.003). Furthermore, depressive mood was significantly more prevalent in the sarcopenia group (P = 0.011). Multiple linear regression analysis showed that the Geriatric Depression Scale score was associated with grip strength (ß = -0.23, P = 0.004) and walking speed (ß = -0.15, P = 0.006), but not skeletal muscle mass index (ß = -0.16, P = 0.142), after controlling for demographic factors, chronic diseases, inflammatory markers and physical activity. CONCLUSIONS: Sarcopenia was associated with depressive mood. In terms of the diagnostic components of sarcopenia, depressive mood was not associated with decreased muscle mass, but was associated with low muscle strength and low physical performance. Geriatr Gerontol Int 2019; 19: 508-512.

Objectively measured physical activity and cognitive function in urban-dwelling older adults.

AIM: Physical activity (PA) and cognition have reportedly been associated with each other. However, it remains to be elucidated what intensities of PA are most strongly associated with cognition. In the current study, we aimed to determine the association between the intensities of objectively measured PA and cognitive function. METHODS: The present study was a cross-sectional analysis of the data obtained at registration in a randomized control trial in Toyota, Japan. Participants were community-dwelling older adults who had cognitive complaints. A battery of neuropsychological and physical assessments was carried out. Daily PA data were collected with the activity monitor. PA was categorized into one of three activity levels defined as light (<3.0 metabolic equivalents; LPA), moderate and vigorous (3.0 metabolic equivalents) activity. Partial correlation analysis was used to investigate the correlation between PA and cognition, with adjustments for age, sex and school years. We then carried out a multiple regression analysis to investigate the association of cognitive performance with PA, adjusting for insulin resistance or depressive mood. RESULTS: Partial correlation adjusted for age, sex and schooling years showed that LPA was significantly correlated with the Digit Symbol Substitution test, Trail Making Test (TMT) part A and TMT-B, whereas moderate and vigorous activity showed no correlations. Multiple regression analysis with several models with different adjustments showed that LPA was associated with the Digit Symbol Substitution test, TMT-A and TMT-B independently from insulin resistance or depressive mood. CONCLUSIONS: In the current study, we found that LPA was significantly associated with the performance of executive functional assessments. Geriatr Gerontol Int 2018; 18: 922-928.

The Soluble VEGF Receptor sFlt-1 Contributes to Impaired Neovascularization in Aged Mice.

The mechanism by which angiogenesis declines with aging is not fully understood. Soluble vascular endothelial growth factor receptor 1 (VEGFR1) form (sFlt1) contributes to endothelial dysfunction in pathological conditions. However, the roles of sFlt1 in ischemia-induced neovascularizationof aged animals have not been investigated. To study aging-related sFlt1 change and its impact on ischemia-induced neovascularization, a hindlimb ischemia model was applied to young and aged mice. Blood flow imaging assay revealed that the blood flow recovery remained impaired throughout the follow-up period. At day 14, immunostaining showed lesser capillary formation in the aged mice. An ELISA showed that the aged mice had increased plasma sFlt-1 levels at indicated time points after surgery. On operative day 4, the aged ischemic muscles had decreased levels of p-VEGFR2 and p-Akt and increased levels of sFlt-1, Wnt5a, and SC35 genes or/and protein as well as increased numbers of inflammatory cells (macrophages and leucocytes) and matrix metalloproteinase-9 activity. Immnunofluorescence showed that Flt-1 was co-localized with CD11b+ macrophages of aged ischemic muscles. Hypoxia stimulated sFlt1 expression in CD11b+ cells of aged bone-marrow (BM), and this effect was diminished by siWnt5a. The cultured medium of aged mice BM-derived CD11b+ cells suppressed human endothelial cell (EC) and endothelial progenitor cell (EPC) angiogenic actions induced by VEGF, and these decreases were improved by treatment with siWnt5a-conditioned medium. Thus, aging appears to decline neovascularization in response to ischemic stress via the VEGFR2/Akt signaling inactivation in ECs and ECPs that is mediated by Wnt5a/SC35 axis activated macrophages-derived sFlt1 production in advanced age.

Mechanisms with clinical implications for atrial fibrillation-associated remodeling: cathepsin K expression, regulation, and therapeutic target and biomarker.

BACKGROUND: The cysteine protease cathepsin K (CatK) has been implicated in the pathogenesis of cardiovascular disease. We sought to determine the link between atrial fibrillation (AF) and plasma CatK levels and to investigate the expression of and therapeutic target for CatK in vivo and in vitro. METHODS AND RESULTS: Plasma CatK and extracellular matrix protein peptides (intact procollagen type I of N-terminal propeptide; carboxyl-terminal telopeptide of type I collagen [ICTP]) were measured in 209 consecutive patients with AF (paroxysmal AF, 146; persistent AF, 63) and 112 control subjects. In addition, the regulation of CatK expression was investigated in vivo and vitro. Patients with AF had higher plasma CatK and ICTP levels than did control subjects. Patients with persistent AF had higher levels of plasma CatK and ICTP than did patients with paroxysmal AF. CatK was correlated with ICTP concentration and left atrial diameter in all subjects. In rabbits, superoxide production, CatK activity, fibrosis, and the levels of atrial tissue angiotensin II, angiotensin type 1 receptor, gp91phox, phospho-p38 mitogen-activated protein kinase, and CatK were greater in those with tachypacing-induced AF than in controls, and these changes were reversed with angiotensin type 1 receptor antagonist. Olmesartan and mitogen-activated protein kinase inhibitor decreased the CatK expression induced by angiotensin II in rat neonatal myocytes. CONCLUSIONS: These data indicated that increased plasma CatK levels are linked with the presence of AF. Angiotensin type 1 receptor antagonist appears to be effective in alleviating atrial fibrosis in a rabbit AF model, partly reducing angiotensin type 1 receptor-p38mitogen-activated protein kinase-dependent and -independent CatK activation, thus preventing AF.