GDNF Promotes Survival and Therapeutic Efficacy of Human Adipose-Derived Mesenchymal Stem Cells in a Mouse Model of Parkinson's Disease.

Early human evidence such as case series or small samples is exploring possible benefits.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Mesenchymal stem cell (MSC)-based regenerative therapy is regarded as a promising strategy for the treatment of Parkinson's disease (PD). However, MSC components may exhibit poor intracranial survivability, particularly in the later stages following cell transplantation, limiting their potential curative effect and also clinical applications. Glial cell line-derived neurotrophic factor (GDNF), which encompasses a variety of transforming growth factor beta super family members, has been reported to enhance motor function and exert neuroprotective effects. However, no previous studies have investigated the effects of GDNF on human primary adipose-derived MSCs (hAMSCs), despite its potential for enhancing stem cell survival and promoting therapeutic efficacy in the treatment of PD. In the present study, we proposed a novel approach for enhancing the proliferative capacity and improving the efficacy of hAMSC treatment. Pre-exposure of engineered hAMSCs to GDNF enhanced the proliferation and differentiation of these stem cells in vitro. In addition, in 6-hydroxydopamine-lesioned mice, a common PD model, intracranial injection of hAMSCs-GDNF was associated with greater performance on behavioral tests, larger graft volumes 5 weeks after transplantation, and higher levels of Nestin, glial fibrillary acidic protein, and Tuj-1 differentiation than those treated with hAMSCs-Vector. Follow

Evidence level

Early human evidence such as case series or small samples is exploring possible benefits.

Browse all related research

Filter the research library by this study's title keywords, author, or publication year.