The study of epigenetic has brought about a deeper understanding of developmental programming through a complex network of modifications involving the DNA. While the DNA sequence remains conservative throughout, the mechanism of epigenetic modification involves changes through histone modification, DNA methylation, and chromatin remodelling. The overall dynamic effect of epigenetic modification allows the gene expression to be altered leading to a diverse phenotypical expression; a functional change in the genome without affecting the DNA. The emergence of nutritional neuroepigenetic serves to bring into focus the impact of nutrition as an environmental agent in regulating gene expression patterns leading to phenotypical expression with profound neurological and cognitive implication in later life. This link is supported by evidence from animal models suggesting that epigenetic marks, which are formed following DNA methylation or histone modification, can induce changes leading to developmental diseases or persist into adulthood. The difficulty in understanding the intrinsic biomolecular correlation between 1) epigenetic modification, 2) nutritional imbalance, and 3) cognitive impairment in an animal based model provides a compelling question regarding the developmental origins of cognitive related diseases. There have been few animal model studies involving the molecular basis of neuroepigenetic dysfunction in the relation to over nutrition or under nutrition. The main criteria in this review will focus on the few animal based studies in nutrition based epigenetic reprogramming and its role in neuroepigenetic dysregulation and cognitive impairment.
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