Human Fetal Cells Rescue Mouse Myelination Defect
Transplanting human fetal cells into the brains of newborn mice lacking myelin leads to widespread myelination, restoration of normal neural function and increased survival, according to research published in the June issue of Cell Stem Cell.
FRIDAY, June 6 (HealthDay News) -- Transplanting human fetal cells into the brains of newborn mice lacking myelin leads to widespread myelination, restoration of normal neural function and increased survival, according to research published in the June issue of Cell Stem Cell.
Martha S. Windrem, from the University of Rochester Medical Center in Rochester, N.Y., and colleagues injected fetal human glial progenitor cells into the brains of neonatal immunodeficient (to avoid rejection) mutant mice lacking myelin. The mice lack full-length myelin basic protein and normally die by 18-21 weeks of age, the authors note.
The researchers found that the transplant led to widespread myelination of the neuraxis, spreading from the brain to the spinal cord and roots. The mice also had greatly increased survival, substantial resolution of their neurological deficits, and normal nodes of Ranvier and transcallosal conduction velocities. The brains of the transplanted mice were chimeras, consisting of murine gray matter but predominantly human white matter glial cells.
"These data demonstrate that the neonatal transplantation of human glial progenitor cells can effectively treat disorders of congenital and perinatal hypomyelination," Windrem and colleagues conclude.
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