Abstract
Fetal growth restriction (FGR) is one of the most important obstetric pathologies. It is frequently caused by placental insufficiency. Previous studies have shown a relationship between FGR and impaired new-born neurodevelopment, although the molecular mechanisms involved in this association have not yet been completely clarified. Reelin is an extracellular matrix glycoprotein involved in development of neocortex, hippocampus, cerebellum and spinal cord. Reelin has been demonstrated to play a key role in regulating perinatal neurodevelopment and to contribute to the emergence and development of various psychiatric pathologies, and its levels are highly influenced by pathological conditions of hypoxia. The purpose of this article is to study whether reelin levels in new-borns vary as a function of severity of fetal growth restriction by gestational age and sex. We sub-grouped fetuses in: normal weight group (Group 1, n = 17), FGR group with normal umbilical artery Doppler and cerebral redistribution at middle cerebral artery Doppler (Group 2, n = 9), and FGR with abnormal umbilical artery Doppler (Group 3, n = 8). Our results show a significant association of elevated Reelin levels in FGR fetuses with cerebral blood redistribution compared to the normal weight group and the FGR with abnormal umbilical artery group. Future research should focus on further expanding the knowledge of the relationship of reelin and its regulated products with neurodevelopment impairment in new-borns with FGR and should include larger and more homogeneous samples and the combined use of different in vivo techniques in neonates with impaired growth during their different adaptive phases.
Highlights
Intrauterine growth restriction is among the most common obstetric syndromes; it can affect 3 to 10% of pregnancies when it is caused by placental insufficiency [1]
The relationship between fetal growth restriction (FGR) and neurodevelopmental impairment is reflected by numerous epidemiological studies showing that affected new-borns (NBs) may present motor and/or cognitive disorders [2,3,4], following the trend reported by Baker in the last century with his theory of developmental origins of health and adult disease [5]
Given the reality of fetuses affected by FGR and impaired neurodevelopment, it was proposed that the concentration of reelin, a protein involved in migration, cortical organization, and synapses during prenatal development of the brain, could vary depending on the type of fetal growth impairment and its adaptive phase
Summary
Intrauterine growth restriction is among the most common obstetric syndromes; it can affect 3 to 10% of pregnancies when it is caused by placental insufficiency [1]. The relationship between fetal growth restriction (FGR) and neurodevelopmental impairment is reflected by numerous epidemiological studies showing that affected new-borns (NBs) may present motor and/or cognitive disorders [2,3,4], following the trend reported by Baker in the last century with his theory of developmental origins of health and adult disease [5]. The relationship between congenital heart disease, which chronically compromises prenatal brain flow, and the development of microcephaly and neurodevelopmental impairment has the same basis [7]. When noxa occurs during the migration phase, different phenotypes result in rodent models [8] and in neonatal models with a prenatal diagnosis of ischaemia by ultrasound [9]. Doppler ultrasound and proton MRI spectroscopy have revealed that NBs with FGR present adaptive brain reorganization, with increased deterioration towards the basal ganglia [11], and altered brain metabolism, with reduced ratios of N-acetyl-aspartate:choline and N-acetyl-aspartate:creatinine [12,13]
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