The salient features of our findings are: (1) BMSC transplantation attenuated HD-induced neuron apoptosis in the spinal cord of rats; (2) NGF was a key factor responsible for the anti-apoptotic capacity of BMSC; (3) BMSC activated Akt/Bad signaling pathway in a NGF/TrkA-dependent manner, resulting in dissociation of Bad/Bcl-xL complex; (4) Pharmacological inhibition of Akt abolished the anti-apoptotic capacity of BMSC and NGF in HD-generated neurotoxic model in vitro. This evidence concerns the gene BCL2L1 and Huntington disease.