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Background/Aim: The cause of fatal neuromuscular amyotrophic lateral sclerosis (ALS) is not known. Materials and Methods: Ninety-day-old superoxide-dismutase-1  G93A  (SOD1  G93A  ) mice demonstrating level 1 paralysis, received 9.0 Gy total body irradiation (TBI) from a cesium source at 340 cGy per minute, and intravenous transplantation with 1×10  6  C57BL/6 green fluorescent protein (GFP)+ donor bone marrow cells. Results: Paralysis-free survival was prolonged in TBI and bone marrow-transplanted SOD1  G93A  mice from 100 to over 250 days (p=0.0018). Other mice transplanted with SOD1  G93A  marrow or marrow treated with the free-radical scavenger MMS350 showed no therapeutic effect. GFP+ macrophage-2 (M 2 ) microglial cells of bone marrow origin, were seen at sites of degenerating anterior horn motor neurons. SOD1  G93A  mice had a disruption in the blood-brain barrier permeability which was reversed by marrow transplant from C57BL/6 mice. SOD1  G93A  marrow showed unexpected robust hematopoiesis in vitro, and radioresistance. Conclusion: After TBI, M 2 microglial cells from transplanted donor marrow extended the paralysis-free interval in SOD1  G93A  mice.

Amelioration of Amyotrophic Lateral Sclerosis in SOD1G93AMice by M2Microglia from Transplanted Marrow

Amelioration of Amyotrophic Lateral Sclerosis in SOD1^G93AMice by M₂Microglia from Transplanted Marrow