MOTHER’S SLEEP APNEA- AUTISM

Abstract

According to scientific data, many psychiatric diseases are the result of a complex interaction between genetics and early life events, in the womb. Sleep Apnea (SA) is characterised by periodic partial or total cessations of breathing during sleep and is becoming more common during pregnancy. SA produces pathological reductions in blood oxygen levels (intermittent hypoxia-IH) leads to poor pregnancy and newborn outcomes. The effects of SA on brain-based behavioural outcomes and associated neuronal function in offspring during pregnancy are unknown¹. The researchers created a rat model of prenatal SA during pregnancy by subjecting dams to IH, an unique attribute of SA, from trimester days 10 to 21, and examining the impacts on the offspring's frontal brain nerve cell structure, synaptic function, and cognitive and behavioural phenotypes at different phases of development. Findings shows prenatal variables creating sexually dimorphic behavioural traits linked with increased (rather than decreased) synapse counts, and they suggest that hyperactivity of the mammalian target of rapamycin (mTOR) pathway is involved in the behavioural abnormalities². These findings have implications for neuropsychiatric illnesses characterised by excessive synapse maintenance, which is thought to be caused, in part, by mostly unknown disturbances to the maternal environment.