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Sci Adv. 2019 Feb 27;5(2):eaau6328. doi: 10.1126/sciadv.aau6328. eCollection 2019 Feb.

Sodium rutin ameliorates Alzheimer's disease-like pathology by enhancing microglial amyloid-β clearance.

Pan RY1,2,3, Ma J3, Kong XX3, Wang XF4, Li SS1,2,3, Qi XL1,2,3, Yan YH5, Cheng J3, Liu Q6, Jin W7, Tan CH4, Yuan Z3,8.

Author information

1
The State Key Laboratory of Brain and Cognitive Sciences, Institute of Biophysics, Chinese Academy of Sciences, Beijing 100101, China.
2
The College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China.
3
The Brain Science Center, Beijing Institute of Basic Medical Sciences, Beijing 100850, China.
4
Department of Natural Medicinal Chemistry, Shanghai Institute of Materia Medica, Chinese Academy of Sciences, Shanghai 201203, China.
5
Department of Physiology, Dalian Medical University, Dalian 116044, China.
6
High Magnetic Field Laboratory, Chinese Academy of Sciences, Hefei, Anhui, 230031, China.
7
Key Laboratory of Animal Ecology and Conservation Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing 100101, China.
8
Center of Alzheimer's Disease, Beijing Institute for Brain Disorders, Beijing 100069, China.

Abstract

The accumulation of aggregated amyloid-β (Aβ) in the brain is the first critical step in the pathogenesis of Alzheimer's disease (AD), which also includes synaptic impairment, neuroinflammation, neuronal loss, and eventual cognitive defects. Emerging evidence suggests that impairment of Aβ phagocytosis and clearance is a common phenotype in late-onset AD. Rutin (quercetin-3-rutinoside) has long been investigated as a natural flavonoid with different biological functions in some pathological circumstances. Sodium rutin (NaR), could promote Aβ clearance by increasing microglial by increasing the expression levels of phagocytosis-related receptors in microglia. Moreover, NaR promotes a metabolic switch from anaerobic glycolysis to mitochondrial OXPHOS (oxidative phosphorylation), which could provide microglia with sufficient energy (ATP) for Aβ clearance. Thus, NaR administration could attenuate neuroinflammation and enhance mitochondrial OXPHOS and microglia-mediated Aβ clearance, ameliorating synaptic plasticity impairment and eventually reversing spatial learning and memory deficits. Our findings suggest that NaR is a potential therapeutic agent for AD.

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