And, agonist of Shh-Smo pathway protects against steroid induced cerebellar injury in neonatal mice
THURSDAY, Oct. 20 (HealthDay News) -- Postnatal glucocorticoid exposure increases the risk of cerebellar growth impairment in preterm neonates; and a small molecular agonist of the Sonic hedgehog-Smoothened (Shh-Smo) signaling pathway (SAG) protects against postnatal glucocorticoid-induced cerebellar injury in neonatal mice, according to two studies published in the Oct. 19 issue of Science Translational Medicine.
Emily W.Y. Tam, M.D., from the University of California in San Francisco, and colleagues investigated whether perinatal glucocorticoid exposure increased the risk of cerebellar growth impairment in 172 preterm neonatal infants, assessed at near birth and near term-equivalent age. After adjusting for associated clinical factors, there was no correlation between prenatal betamethasone and changes in cerebellar volume, but postnatal exposure to hydrocortisone or dexamethasone correlated with impaired cerebellar, but not cerebral, growth.
Vivi M. Heine, Ph.D., from the University of California in San Francisco and colleagues investigated whether systemic administration of SAG prevents postnatal glucocorticoid-induced cerebellar injury in neonatal mice. The investigators found that transient (one-week-long) SAG treatment of neonatal animals was well tolerated and did not promote tumor formation, but prevented the neurotoxic effects of glucocorticoids and did not interfere with the beneficial effects of glucocorticoids on lung maturation.
"These findings suggest that a small-molecule agonist of Smo has potential as a neuroprotective agent in neonates at risk for glucocorticoid-induced neonatal cerebellar injury," Heine and colleagues write.
Abstract - Tam
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Abstract - Heine
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