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.
|Original language||English (US)|
|Number of pages||9|
|Journal||International Journal of Developmental Neuroscience|
|State||Published - Oct 2013|
Bibliographical noteFunding Information:
We would like to thank Debra Okafor, Zivjena Vucetic, and Ryan Cunningham for their assistance in completion of the newly reported data in this paper. Supported by MH087978, MH091372, and a Brain and Behavior Research Foundation (formerly NARSAD) Young Investigator Grant.
- DNA methylation
- Intrauterine growth restriction