Related Experiment Video
Updated: Jun 6, 2026

Systemic Injection of Neural Stem/Progenitor Cells in Mice with Chronic EAE
Published on: April 15, 2014
Inflammatory changes induced by transplanted neural precursor cells in a multiple sclerosis model
Angeliki Giannakopoulou1, Nikolaos Grigoriadis, Eleni Polyzoidou
1Second Department of Neurology, AHEPA University Hospital, Aristotle University of Thessaloniki, Macedonia, Greece.
Recent studies on neural precursor cell (NPC) transplantation in multiple sclerosis animal models reveal that these cells exert their therapeutic effect mainly because of immunomodulation rather than cell replacement. In this study intraventricularly transplanted NPCs in mice, induced experimental autoimmune encephalomyelitis, the animal model of multiple sclerosis, improved the clinical symptoms and suppressed inflammation in the brain by enhancing the apoptosis of inflammatory cells. However, the same treatment failed to reduce significantly the inflammatory cells in the spinal cord, the pathology of which predominantly determines the clinical manifestation of experimental autoimmune encephalomyelitis. Our findings suggest that immunosuppression is rather a local phenomenon and thus, bystander neuroprotective mechanisms triggered by NPC intraventricular transplantation should be accountable for their therapeutic effect.
Recent studies on neural precursor cell (NPC) transplantation in multiple sclerosis animal models reveal that these cells exert their therapeutic effect mainly because of immunomodulation rather than cell replacement. In this study intraventricularly transplanted NPCs in mice, induced experimental autoimmune encephalomyelitis, the animal model of multiple sclerosis, improved the clinical symptoms and suppressed inflammation in the brain by enhancing the apoptosis of inflammatory cells. However, the same treatment failed to reduce significantly the inflammatory cells in the spinal cord, the pathology of which predominantly determines the clinical manifestation of experimental autoimmune encephalomyelitis. Our findings suggest that immunosuppression is rather a local phenomenon and thus, bystander neuroprotective mechanisms triggered by NPC intraventricular transplantation should be accountable for their therapeutic effect.

