Bidirectional longitudinal associations between balance performance and depressive symptoms in older adults: A cross-lagged panel model.

BACKGROUND: Evidence on the temporal sequences between balance and depressive symptoms is limited, and no studies have compared the strength of each direction. This study aimed to assess the association between balance performance and depressive symptoms among community-dwelling older adults, and further to explore the driving factors in the dynamic association. METHODS: Data were obtained from the English Longitudinal Study of Aging (ELSA). Overall, 3971 community-residing adults aged 50 years or older were assessed at 2004/05, 2008/09, and 2012/13. Balance was measured using three progressively more difficult tasks (side-by-side, semi-tandem, and full-tandem). Depressive symptoms were determined with a dichotomous eight-item version of the Center for Epidemiologic Studies Depression Scale (CES-D). Cross-lagged panel models were used to test the reciprocal relationships between balance and depressive symptoms. RESULTS: Our analyses revealed that earlier poorer balance predicted later worse depressive symptoms consistently across waves (ßW2-W4 = -0.058, P < .05, ßW4-W6 = -0.067, P < .001). Conversely, the higher scores of depressive symptoms at wave 4 predicted lower level of balance at wave 6 (ßW4-W6 = -0.038, P = .018). The cross-lagged effects of balance on depressive symptoms were over all stronger than the reverse effects. CONCLUSIONS: These findings add novel insights into the temporal directionality of balance and depressive symptoms among community-dwelling older adults, and suggest that a predominance of balance disorder effects. Interventional strategy should aim to increase balance ability from earlier stages to promote successful aging.

Phagocytosis of Advanced Glycation End Products (AGEs) in Macrophages Induces Cell Apoptosis.

Advanced glycation end products (AGEs) are the products of a series of nonenzymatic modifications of proteins by reducing sugars. AGEs play a pivotal role in development of diabetic complications and atherosclerosis. Accumulation of AGEs in a vessel wall may contribute to the development of vascular lesions. Although AGEs have a diverse range of bioactivities, the clearance process of AGEs from the extracellular space, including the incorporation of AGEs into specific cells, subcellular localization, and the fate of AGEs, remains unclear. In the present study, we examined the kinetics of the uptake of AGEs by mouse macrophage J774.1 cells in vitro and characterized the process. We demonstrated that AGEs bound to the surface of the cells and were also incorporated into the cytoplasm. The temperature- and time-dependent uptake of AGEs was saturable with AGE concentration and was inhibited by cytochalasin D but not chlorpromazine. We also observed the granule-like appearance of AGE immunoreactivity in subcellular localizations in macrophages. Higher concentrations of AGEs induced intracellular ROS and 4-HNE, which were associated with activation of the NF-κB pathway and caspase-3. These results suggest that incorporation of AGEs occurred actively by endocytosis in macrophages, leading to apoptosis of these cells through NF-κB activation.