The Molecular Mechanisms Underlying Sleep Deprivation and Impaired Fetal Neurodevelopment Pearse O’Malley
Sleep deprivation (SD) has been implicated in several short-term and long-term cognitive deficits in organisms. While most research has focused on adult organisms, there is increasing concern surrounding the effects of pregnant individuals’ SD on the neurodevelopment of their fetus. A relationship between sleep, stress, and the immune system has previously been established, but the role of SD in causing inflammation was unclear. Baratta et al. (2020) examined the molecular pathways affected by maternal SD and the consequences for the fetus by inducing SD in pregnant mice and obtaining tissue and plasma samples from the mother and fetus. Corticosterone and kynurenic acid (KYNA) were used as markers of stress and impaired metabolism due to SD, respectively, with greater corticosterone levels in the sleep-deprived mice that did not recover from SD and greater KYNA accumulation, correlating to increased KYNA accumulation in the fetal brain. The results indicate that the stress response elicited from maternal SD is related to fetal brain KYNA accumulation, which is associated with weakened memory and learning abilities in the offspring, thus highlighting the dangerous effects of maternal SD on fetal neurodevelopment. Key words: Sleep deprivation (SD), kynurenine pathway (KP), maternal stress, corticosterone, pregnancy
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