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Assesses neuronal injury biomarkers in infants from mothers with sleep-disordered breathing, suggesting early neurodevelopment risk.
Sleep-disordered breathing (SDB) during pregnancy may compromise fetal development and brain maturation. Ubiquitin C-terminal hydrolase-L1 (UCH-L1) and glial fibrillary acidic protein (GFAP) are biomarkers of neuronal injury and cellular stress and may provide insight into fetal vulnerability in this context. UCH-L1 and GFAP concentrations were measured in umbilical cord blood from 85 neonates born to women who underwent hospital-based polysomnography during the third trimester. The apnea-hypopnea index (AHI, and rapid eye movement (REM)-AHI)) and mean nocturnal oxygen saturation (mSaO 2 ) were assessed. SDB phenotypes (OSA n = 14; REM-OSA n = 25; and mSaO₂ ≤95% n = 31) showed no significant differences in UCH-L1 or GFAP compared with controls. However, UCH-L1 levels were higher in neonates exposed to shorter apnea-hypopnea (AH) events, and both maternal AH length and mSaO 2 were negatively correlated with UCH-L1 concentrations. Overall, maternal SDB was not broadly associated with differences in UCH-L1 and GFAP levels. Nevertheless, elevated neonatal UCH-L1 linked to non-traditional metrics, such as AH length and mSaO₂, suggests fetal cellular stress and highlights its potential as an early biomarker of neurodevelopment risk.
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Cànaves‐Gómez et al. (2026) studied this question.
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