Another aspect related to environmental influences is obesity. Greenfield et al. (2004) examined the causality of the C-reactive protein (CRP) in heart disease and obesity by looking at the relationship between CRP, accurately measured body fat, lipids, apolipoproteins, blood pressure and environmental and behavioral factors that are independent of genetic influences in 194 healthy female twins. Results revealed that CRP was strongly related to total and central abdominal obesity, blood pressure and lipid levels that were independent of genetic influences on CRP and obesity. These relationships are likely to contribute significantly to prospective associations between CRP, type 2 diabetes and coronary events (Greenfield et al., 2004).
On the other hand, there is a significant association between epigenetics and aging. Several reports indicate that there is an age-dependent decrease of global DNA methylation and concurrent sight specific hyper-mythylation (Rampersaud, Kauwell, Hutson, Cerda & Bailey, 2000). Epigenetic modification can mediate environmental influences on gene expression; DNA hypo-methylation observed with aging can contribute to disease in the elderly.
A greater understanding of epigenetic mechanism provides extensive opportunities for identifying the genetic and environmental factors that contribute to disease risks (Foley et al., 2009). Furthermore, stress-induced epigenetic modification may emerge during aging. Amusingly; the DNA methylation alterations observed with aging appear to be similar to the DNA methylation alterations in cancer development (Esteller, 2008; Kulis and Esteller, 2010). There is a need for further exploration of the alterations in specific epigenetic alterations in aging MZ twin pairs to elucidate the effect of the environmental factors and epigenetic modifications mechanism, while controlling the genetic variables.
Finally, stress is one of the most important and significant players that bridge the environment to the genes through epigenetic modifications. Ample of evidence from animal stress models indicate that stressful life event results in epigenetic modification in the brain, further more reveal the plasticity of the epigenome across the lifespan. For instance, It is well established that depression commonly occurs in the aftermath of chronic stress (Sheline, Gado, & Kraemer, 2003), where chronic stress can confer enduring epigenetic modifications that contribute to depression (Tsankova et al., 2006).
Tsankova et al. (2006) found that chromatin remodeling of the BDNF gene in the hippocampus may contribute to stress-induced depression by altering neural plasticity. They administered chronic social defeat stress followed by chronic tricyclic antidepressant to mice. They analysed adaptations at the levels of gene expression and chromatin remodeling of five brain-derived neurotrophic factor (BDNF) in the hippocampus.
They found that mice displaying the depressive-like phenotype exhibit reductions in hippocampal BDNF gene expression that is accompanied by persistent histone modifications of the BDNF gene. While, chronic tricyclic antidepressant reversed this downregulation, it also increased histone acetylation at these promoters. This study emphasizes an important role for histone remodeling in the pathophysiology and treatment of depression and highlight the therapeutic potential for histone methylation and deacetylation inhibitors in depression (Tsankova et al., 2006).
This suggests that such epigenetic modification induced by stress may increase inflammatory mediators within the brain. Furthermore, research from animal models indicate that psychological stress triggered by stressful events induce a distinct GR-dependent histone modifications in mature dentate gyrus granule neurons in the hippocampus that may participate in the behavioral adaptation of the organism to this event (Bilang-Bleuel et al., 2005). These changed in the dentate gyrus result from chromatin remodeling.
Along the same lines, Hunter et al. (2009) examined the effects of stress, stress duration, corticosterone administration, and fluoxetine treatment on the levels of hippocampal histone modifications. They found that acute stress increased the levels of histone methylation in the dentate gyrus. Chronic restraint stress resulted in histone modification. This chromatin remodeling within hippocampus produced by stress enhances the knowledge regarding the interplay of stress and hippocampal gene expression, and reveal the outlines of a potential chromatin stress response that may be diminished or degraded by chronic stress
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