Gestational overgrowth and undergrowth affect neurodevelopment: similarities and differences from behavior to epigenetics |
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Authors: | Nicola M. Grissom Teresa M. Reyes |
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Affiliation: | Institute of Translational Medicine and Therapeutics, Perelman School of Medicine, University of Pennsylvania, 3400 Civic Center Boulevard, Philadelphia, PA 19104, United States |
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Abstract: | The size of an infant at birth, a measure of gestational growth, has been recognized for many years as a biomarker of future risk of morbidity. Both being born small for gestational age (SGA) and being born large for gestational age (LGA), are associated with increased rates of obesity and metabolic disorder, as well as a number of mental disorders including attention deficit/hyperactivity disorder, autism, anxiety, and depression. The common risks raise the question of what neurobiological mechanisms are altered in SGA and LGA offspring. Here we review recent findings allowing for direct comparison of neurobiological outcomes of SGA and LGA in human and animal models. We also present new data highlighting similarities and differences in behavior and neurobiology in our mouse models of SGA and LGA. Overall, there is significant data to support aberrant epigenetic mechanisms, particularly related to DNA methylation, in the brains of SGA and LGA offspring, leading to disruptions in the cell cycle in development and gene expression in adulthood. |
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Keywords: | ADHD, attention deficit/hyperactivity disorder BDNF, brain-derived neurotrophic factor CNS, central nervous system DA, dopamine DAT, dopamine transporter GWG, gestational weight gain HF, high-fat IUGR, intrauterine growth restriction LGA, large for gestational age LP, low-protein MOR, mu-opioid receptor NAc, nucleus accumbens PENK, preproenkephalin PFC, prefrontal cortex PI3K, phosphoinositide 3-kinase SGA, small for gestational age TH, tyrosine hydroxylase VTA, ventral tegmental area |
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