Brain damage associated with oxygen deprivation in neonatal mice can be partly reversed with specific pharmacological intervention, reports a study published online this week in Nature Neuroscience. This work identifies a possible new therapeutic target for drug development to promote myelin formation in the neonatal and adult brain.
White matter injury, as seen in cerebral palsy or in oxygen deprivation before or during birth is characterized by the inability of oligodendrocytes, a type of neuronal support cell, to change into myelin-forming cells; there is currently no therapy to overcome this deficit. A similar deficit in the ability to form new myelin cells is seen in adults suffering from multiple sclerosis.
David Rowitch and colleagues found that a protein called Axin2 is expressed in white matter injuries in human neonates and in multiple sclerosis lesions. The authors tested a drug that stabilizes the Axin protein in oxygen-deprived neonatal mice and found that it can promote oligodendrocyte function. This treatment also promoted re-myelination of the white matter tract in cultured cells from mice following hypoxic injury.