title: Salidroside reduces tau hyperphosphorylation via up-regulating GSK-3β phosphorylation in a tau transgenicDrosophilamodel of Alzheimer's disease.
abstract: BACKGROUND
  Alzheimer's disease (AD) is an age-related and progressive neurodegenerative disease that causes substantial public health care burdens. Intensive efforts have been made to find effective and safe treatment against AD. Salidroside (Sal) is the main effective component ofRhodiola rosea L., which has several pharmacological activities. The objective of this study was to investigate the efficacy of Sal in the treatment of AD transgenicDrosophilaand the associated mechanisms.
  
  
  METHODS
  We used tau transgenicDrosophilaline (TAU) in which tau protein is expressed in the central nervous system and eyes by the Gal4/UAS system. After feeding flies with Sal, the lifespan and locomotor activity were recorded. We further examined the appearance of vacuoles in the mushroom body using immunohistochemistry, and detected the levels of total glycogen synthase kinase 3β (t-GSK-3β), phosphorylated GSK-3β (p-GSK-3β), t-tau and p-tau in the brain by western blot analysis.
  
  
  RESULTS
  Our results showed that the longevity was improved in salidroside-fedDrosophilagroups as well as the locomotor activity. We also observed less vacuoles in the mushroom body, upregulated level of p-GSK-3β and downregulated p-tau following Sal treatment.
  
  
  CONCLUSIONS
  Our data presented the evidence that Sal was capable of reducing the neurodegeneration in tau transgenicDrosophilaand inhibiting neuronal loss. The neuroprotective effects of Sal were associated with its up-regulation of the p-GSK-3β and down-regulation of the p-tau.
authors.affiliation: Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin Er Road, Shanghai, 200025 China.|Laboratory of Neurodegenerative Diseases, Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS) & Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, 200025 China.
authors.forename: Bei
authors.initials: B
authors.lastname: Zhang
authors.affiliation: Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin Er Road, Shanghai, 200025 China.
authors.forename: Qiongqiong
authors.initials: Q
authors.lastname: Li
authors.affiliation: Laboratory of Neurodegenerative Diseases, Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS) & Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, 200025 China.
authors.forename: Xingkun
authors.initials: X
authors.lastname: Chu
authors.affiliation: Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin Er Road, Shanghai, 200025 China.
authors.forename: Suya
authors.initials: S
authors.lastname: Sun
authors.affiliation: Department of Neurology and Institute of Neurology, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, 197 Ruijin Er Road, Shanghai, 200025 China.|Laboratory of Neurodegenerative Diseases, Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS) & Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, 200025 China.
authors.forename: Shengdi
authors.initials: S
authors.lastname: Chen
keywords: Alzheimer’s disease; Drosophila; Glycogen synthase kinase 3β; Salidroside; Tau