Antioxidants (Basel)
December 2024
Neonatal brain injury remains a significant issue with limited treatment options. This study investigates the potential of the endogenous neurosteroid dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) as neuroprotective agents, building on evidence of their mechanisms in adult brain injury models. The primary objective was to evaluate their neuroprotective and anti-oxidative properties in a mouse model of neonatal hypoxic-ischemic brain injury.
View Article and Find Full Text PDFIntroduction: There are conflicting data on the association between postnatal cytomegalovirus (CMV) infection and growth and cognitive outcome in very preterm infants. The aim of the current study was to systematically evaluate the effect of postnatal CMV infection on growth and cognitive outcome in an unselected, contemporary cohort of very preterm infants.
Methods: Infants <32 gestational weeks (2011-2018) were screened for postnatal CMV infection.
Why severe injury to the central nervous system (CNS) triggers the development of large neurogenic heterotopic ossifications (NHOs) within periarticular muscles remains unknown. We report that spinal cord injury (SCI) triggers a rapid corticosterone spike in mice, which is causal for NHO development because treatments with corticosterone or the synthetic glucocorticoid (GC) receptor (GR) agonist dexamethasone are sufficient to trigger heterotopic ossification and upregulate the expression of osteoinductive and osteogenic differentiation genes in injured muscles even without SCI. The central role for GR signaling in causing NHO is further demonstrated in mice deleted for the GR gene (Nr3c1), which no longer develop NHO after SCI.
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