Therapeutic potentials of human adipose-derived stem cells on the mouse model of Parkinson's disease

Neurobiol Aging. 2015 Oct;36(10):2885-92. doi: 10.1016/j.neurobiolaging.2015.06.022. Epub 2015 Jun 24.


The treatment of Parkinson's disease (PD) using stem cells has long been the focus of many researchers, but the ideal therapeutic strategy has not yet been developed. The consistency and high reliability of the experimental results confirmed by animal models are considered to be a critical factor in the stability of stem cell transplantation for PD. Therefore, the aim of this study was to investigate the preventive and therapeutic potential of human adipose-derived stem cells (hASC) for PD and was to identify the related factors to this therapeutic effect. The hASC were intravenously injected into the tail vein of a PD mouse model induced by 6-hydroxydopamine. Consequently, the behavioral performances were significantly improved at 3 weeks after the injection of hASC. Additionally, dopaminergic neurons were rescued, the number of structure-modified mitochondria was decreased, and mitochondrial complex I activity was restored in the brains of the hASC-injected PD mouse model. Overall, this study underscores that intravenously transplanted hASC may have therapeutic potential for PD by recovering mitochondrial functions.

Keywords: 6-OHDA; Human adipose-derived stem cells; Mitochondria; Parkinson's disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adipocytes / cytology*
  • Animals
  • Disease Models, Animal
  • Dopaminergic Neurons / pathology
  • Electron Transport Complex I / deficiency
  • Humans
  • Male
  • Mice, Inbred C57BL
  • Mitochondria / pathology
  • Mitochondrial Diseases / etiology
  • Mitochondrial Diseases / therapy
  • Oxidopamine
  • Parkinson Disease / complications
  • Parkinson Disease / pathology
  • Parkinson Disease / prevention & control
  • Parkinson Disease / therapy*
  • Stem Cell Transplantation / methods*
  • Stem Cells*


  • Oxidopamine
  • Electron Transport Complex I

Supplementary concepts

  • Mitochondrial complex I deficiency