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Epigenetics differences in older twin sets, different disease risk during their lifespan CLICK HERE FOR MORE ON THIS PAPER………………….
Epigenetics differences in older twin sets, different disease risk during their lifespan
Q6: Explain why DNA differs more significantly in older twin sets than younger twin sets.
Discuss how genetically identical twins can have different disease risk during their lifespan
What are the implications for reducing disease risk?
Introduction
             Monozygotic (MZ) twins are derived from the same single-cell zygote formed from the fusion of one egg and one sperm. In MZ twins, the inner cell mass of the blastocyst splint into two during the early cell divisions, which gave rise to two embryos that are genetically identical. The study of MZ twins offer fascinating potential which help researchers explore the link between the sequence of the genotype and the phenotype (Carey, 2011). Although MZ are genetically identical, both twins may have different diseases at different times, or so called -twin discordance (Carey, 2011).
          Therefore, the purpose of this paper is to discuss how DNA differs in older twin sets than younger twin sets, and then differences in disease risk during their lifespan will be discussed. Finally, implications for reducing disease risk will be addressed.
DNA differs in older twin sets than younger twin sets
        Monozygotic twins—are identical at the DNA sequence level, but studies have found some phenotypic differences of DNA methylation and histone modification profiles that may be consequences of different exposures to environmental stressors and might affect their susceptibility to different diseases, such as cancer or autoimmune disorders (Kaminsky et al., 2009; Fraga et al, 2005; Javierre et al, 2010).
             There is a prevalent epigenetic drift in monozygotic twins in relation to one another with advancing age (Fraga et al., 2005). Fraga et al. (2005) investigated both global and locus-specific differences in DNA methylation and histone acetylation in identical twins of various ages. Their results revealed that young identical twin pairs are essentially identical in their epigenetic markings, while older identical twin pairs demonstrate significant variations in epigenetic differences in DNA methylation and histone modification. These differential markers between twins are distributed throughout their genomes, affecting repeat DNA sequences and single-copy genes, and have an important impact on gene expression. Interestingly, Variations in gene expression in older twin pairs were four times greater than those observed in young twin pairs.  They found that that these epigenetic modifications were more distinctive in older MZ twins who had different lifestyles, and had spent less of their lives together, emphasizing the significant role of environmental factors in translating a common genotype into a different phenotype.
        In a subsequent study, Martin (2005) reported epigenetic shifts in these aging identical twins could have arisen through endogenous, stochastic mechanisms, independent of environmental perturbations, or could have resulted from such environmental perturbations. These results represent the most comprehensively detailed results of age-associated epigenetic alterations in MZ twins of human subjects.   
              Along the same lines, Talens et al. (2012) conducted a recent study to investigate the occurrence of epigenetic changes over the adult lifespan in monozygotic twin pairs (N=230, 18-89 years). They examined the global DNA methylation difference and found there was more variation within old MZ-pair as compared with young MZ pairs. Furthermore, elderly twins revealed similar pattern of variations in DNA methylation after 10 years follow-up. They concluded that the age-related increase in methylation variation was generally related to the distinct environmental factors for which familial factors may play a more important role. In conclusion, sustained epigenetic differences arise from early adulthood to old age and contribute to an increasing epigenetic variation of MZ twins during aging (Talens et al., 2012) 
             One must note that discordance for numerous multifaceted diseases are not necessarily associated aging. Kaprio et al. (1992) studied the cumulative incidence, concordance rate, and heritability for diabetes mellitus in a nationwide cohort of 13,888 twin pairs of the same sex in Finland. They found that the concordance rate for Type 1 diabetes was higher among monozygotic than dizygotic in the fist and second decade of life. They concluded that heritability for Type 1 diabetes was greater than that for Type 2 where both genetic and environmental effects seemed to play a significant role (Kaprio et al. 1992). On the other hand, Bergem and collegues (1997), compared the relative importance of heredity and environment in the development of Alzheimer disease and vascular dementia. They found that the concordance of Alzheimer’s disease could be as high as 83% at a later age.
          Collectively, epigenetic changes are not restricted to the prenatal period. Monozygotic twins experience an epigenetic drift in relation to one another with advancing age (Fraga et al., 2005).  Differences in epigenetic modifications are influenced by decreasing amounts of time shared together and behavioral differences (Fraga et al., 2005). Additionally, MZ twins provide a unique model which explains how genetically identical twins exhibit differences, and this model lends it self to future research that address the role of epigenetic modifications in the establishment of the phenotype (Petronis wt al., 2003; Wong, Gottesman, and Petronis, 2005).
Differences in disease risk during life span
      Discordance of diseases in MZ twins
        Identification of genes predisposing their carrier to complex diseases is a much more complicated task than finding genes involved in simple mendelian diseases. The dynamic epigenetic mechanisms provide an alternative explanation for some of the features of complex diseases, which include late onset, gender effects, parents of origin effect, discordance of MZ twins, and fluctuation of symptoms in complex diseases (Petronis, 2001).MZ twins share the same genotype because they are derived from the same zygote. However, monozygotic twin have several phenotypic differences that determines susceptibility to diseases. Recent studies suggest that phenotypic discordance between monozygotic twins is at least to some extent due to epigenetic factors that change over the lifetime of a multi-cellular organism. Acute environmental factors are directly associated with epigenetic-dependent disease phenotypes, as demonstrated by the increased CpG-island promoter hyper-methylation of tumor suppressor genes in the normal oral mucosa of smokers (Poulsen, Esteller, Vaag, and Fraga, 2007).  MZ twins who are discordant for disease are an excellent example of how genetically identical individuals can exhibit differences and represent a unique model for studying the contribution and role of environmental factors in disease development. Since monozygotic twins are genetically identical they are considered ideal experimental models for studying the role of environmental factors as determinants of complex diseases and phenotypes (Poulsen, Esteller, 

Epigenetics differences in older twin sets, different disease risk during their lifespan

CLICK HERE FOR MORE ON THIS PAPER………………….

Epigenetics differences in older twin sets, different disease risk during their lifespan
Q6: Explain why DNA differs more significantly in older twin sets than younger twin sets.
Discuss how genetically identical twins can have different disease risk during their lifespan
What are the implications for reducing disease risk?
Introduction
             Monozygotic (MZ) twins are derived from the same single-cell zygote formed from the fusion of one egg and one sperm. In MZ twins, the inner cell mass of the blastocyst splint into two during the early cell divisions, which gave rise to two embryos that are genetically identical. The study of MZ twins offer fascinating potential which help researchers explore the link between the sequence of the genotype and the phenotype (Carey, 2011). Although MZ are genetically identical, both twins may have different diseases at different times, or so called -twin discordance (Carey, 2011).
          Therefore, the purpose of this paper is to discuss how DNA differs in older twin sets than younger twin sets, and then differences in disease risk during their lifespan will be discussed. Finally, implications for reducing disease risk will be addressed.
DNA differs in older twin sets than younger twin sets
        Monozygotic twins—are identical at the DNA sequence level, but studies have found some phenotypic differences of DNA methylation and histone modification profiles that may be consequences of different exposures to environmental stressors and might affect their susceptibility to different diseases, such as cancer or autoimmune disorders (Kaminsky et al., 2009; Fraga et al, 2005; Javierre et al, 2010).
             There is a prevalent epigenetic drift in monozygotic twins in relation to one another with advancing age (Fraga et al., 2005). Fraga et al. (2005) investigated both global and locus-specific differences in DNA methylation and histone acetylation in identical twins of various ages. Their results revealed that young identical twin pairs are essentially identical in their epigenetic markings, while older identical twin pairs demonstrate significant variations in epigenetic differences in DNA methylation and histone modification. These differential markers between twins are distributed throughout their genomes, affecting repeat DNA sequences and single-copy genes, and have an important impact on gene expression. Interestingly, Variations in gene expression in older twin pairs were four times greater than those observed in young twin pairs.  They found that that these epigenetic modifications were more distinctive in older MZ twins who had different lifestyles, and had spent less of their lives together, emphasizing the significant role of environmental factors in translating a common genotype into a different phenotype.
        In a subsequent study, Martin (2005) reported epigenetic shifts in these aging identical twins could have arisen through endogenous, stochastic mechanisms, independent of environmental perturbations, or could have resulted from such environmental perturbations. These results represent the most comprehensively detailed results of age-associated epigenetic alterations in MZ twins of human subjects.   
              Along the same lines, Talens et al. (2012) conducted a recent study to investigate the occurrence of epigenetic changes over the adult lifespan in monozygotic twin pairs (N=230, 18-89 years). They examined the global DNA methylation difference and found there was more variation within old MZ-pair as compared with young MZ pairs. Furthermore, elderly twins revealed similar pattern of variations in DNA methylation after 10 years follow-up. They concluded that the age-related increase in methylation variation was generally related to the distinct environmental factors for which familial factors may play a more important role. In conclusion, sustained epigenetic differences arise from early adulthood to old age and contribute to an increasing epigenetic variation of MZ twins during aging (Talens et al., 2012) 
             One must note that discordance for numerous multifaceted diseases are not necessarily associated aging. Kaprio et al. (1992) studied the cumulative incidence, concordance rate, and heritability for diabetes mellitus in a nationwide cohort of 13,888 twin pairs of the same sex in Finland. They found that the concordance rate for Type 1 diabetes was higher among monozygotic than dizygotic in the fist and second decade of life. They concluded that heritability for Type 1 diabetes was greater than that for Type 2 where both genetic and environmental effects seemed to play a significant role (Kaprio et al. 1992). On the other hand, Bergem and collegues (1997), compared the relative importance of heredity and environment in the development of Alzheimer disease and vascular dementia. They found that the concordance of Alzheimer’s disease could be as high as 83% at a later age.
          Collectively, epigenetic changes are not restricted to the prenatal period. Monozygotic twins experience an epigenetic drift in relation to one another with advancing age (Fraga et al., 2005).  Differences in epigenetic modifications are influenced by decreasing amounts of time shared together and behavioral differences (Fraga et al., 2005). Additionally, MZ twins provide a unique model which explains how genetically identical twins exhibit differences, and this model lends it self to future research that address the role of epigenetic modifications in the establishment of the phenotype (Petronis wt al., 2003; Wong, Gottesman, and Petronis, 2005).
Differences in disease risk during life span
      Discordance of diseases in MZ twins

        Identification of genes predisposing their carrier to complex diseases is a much more complicated task than finding genes involved in simple mendelian diseases. The dynamic epigenetic mechanisms provide an alternative explanation for some of the features of complex diseases, which include late onset, gender effects, parents of origin effect, discordance of MZ twins, and fluctuation of symptoms in complex diseases (Petronis, 2001).MZ twins share the same genotype because they are derived from the same zygote. However, monozygotic twin have several phenotypic differences that determines susceptibility to diseases. Recent studies suggest that phenotypic discordance between monozygotic twins is at least to some extent due to epigenetic factors that change over the lifetime of a multi-cellular organism. Acute environmental factors are directly associated with epigenetic-dependent disease phenotypes, as demonstrated by the increased CpG-island promoter hyper-methylation of tumor suppressor genes in the normal oral mucosa of smokers (Poulsen, Esteller, Vaag, and Fraga, 2007).  MZ twins who are discordant for disease are an excellent example of how genetically identical individuals can exhibit differences and represent a unique model for studying the contribution and role of environmental factors in disease development. Since monozygotic twins are genetically identical they are considered ideal experimental models for studying the role of environmental factors as determinants of complex diseases and phenotypes (Poulsen, Esteller, 

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