Dietary diversity offsets the adverse mortality risk among older indigenous Taiwanese.

BACKGROUND AND OBJECTIVES: The extent to which health and survival inequality between indigenous and nonindigenous older Taiwanese is associated with diet is uncertain. METHODS AND STUDY DESIGN: Participants from the Elderly Nutrition and Health Survey in Taiwan (1999-2000) formed this cohort. Dietary information was collected by 24-hr recall and simplified food frequency questionnaire. Dietary quality was assessed by dietary diversity score (DDS, 0-6). Annual medical service utilization and expenditure were derived from National Health Insurance claims until 2006. Survivorship was ascertained from the National Death Registry until 2008. Cox proportional- hazards models were used to determine the association between aboriginality and mortality in conjunction with dietary diversity. RESULTS: Indigenes (n=156) compared with nonindigenes (n=1182) significantly differed in socio-demography, behaviors and chronic disease prevalences. For up to 8 years, indigenes had a higher mortality rate (46.2% vs 33.6%, p=0.003). Indigenes' nutrient intakes were less for polyunsaturated fat, dietary fiber, vitamins and minerals (but more sodium); food intakes more for meat, with less cooking oil, dairy products and fruits; and a lower DDS, (3.61 vs 4.54). They had a 41% higher mortality risk (HR: 1.41, 95% CI: 1.09-1.81, p=0.008). Control for demographic variables did not change the findings. However, the increase in HR was substantially attenuated by the inclusion of DDS (HR: 1.15, 95% CI: 0.88-1.49, p=0.316). There was no significant interaction between aboriginality and DDS on mortality (p=0.673). CONCLUSIONS: Older indigenous Taiwanese have a higher mortality risk than their majority counterparts. Irrespective of aboriginality, the more diverse diet is associated with a lower risk of mortality.

Cell-specific Nav1.6 knockdown reduced astrocyte-derived Aß by reverse Na+-Ca2+ transporter-mediated autophagy in alzheimer-like mice.

INTRODUCTION: Nav1.6 is closely related to the pathology of Alzheimer's Disease (AD), and astrocytes have recently been identified as a significant source of ß-amyloid (Aß). However, little is known about the connection between Nav1.6 and astrocyte-derived Aß. OBJECTIVE: This study explored the crucial role of Nav1.6 in mediated astrocyte-derived Aß in AD and knockdown astrocytic Nav1.6 alleviates AD progression by promoting autophagy and lysosome-APP fusion. METHODS: A mouse model for astrocytic Nav1.6 knockdown was constructed to study the effects of astrocytic Nav1.6 on amyloidosis. The role of astrocytic Nav1.6 on autophagy and lysosome-APP(amyloid precursor protein) fusion was used by transmission electron microscope, immunostaining, western blot and patch clamp. Glial cell activation was detected using immunostaining. Neuroplasticity and neural network were assessed using patch-clamp, Golgi stain and EEG recording. Behavioral experiments were performed to evaluate cognitive defects. RESULTS: Astrocytic Nav1.6 knockdown reduces amyloidosis, alleviates glial cell activation and morphological complexity, improves neuroplasticity and abnormal neural networks, as well as promotes learning and memory abilities in APP/PS1 mice. Astrocytic Nav1.6 knockdown reduces itself-derived Aß by promoting lysosome- APP fusion, which is related to attenuating reverse Na+-Ca2+ exchange current thus reducing intracellular Ca2+ to facilitate autophagic through AKT/mTOR/ULK pathway. CONCLUSION: Our findings unveil the crucial role of astrocyte-specific Nav1.6 in reducing astrocyte-derived Aß, highlighting its potential as a cell-specific target for modulating AD progression.