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Epigenetics of early child development.

Murgatroyd C, Spengler D - Front Psychiatry (2011)

Bottom Line: Here we will review recent studies performed with the common aim of understanding the effects of the early environment in shaping brain development and discuss the newly developing role of epigenetic mechanisms in translating early life conditions into long-lasting changes in gene expression underpinning brain functions.Particularly, we argue that epigenetic mechanisms can mediate the gene-environment dialog in early life and give rise to persistent epigenetic programming of adult physiology and dysfunction eventually resulting in disease.Understanding how early life experiences can give rise to lasting epigenetic marks conferring increased risk for mental disorders, how they are maintained and how they could be reversed, is increasingly becoming a focus of modern psychiatry and should pave new guidelines for timely therapeutic interventions.

View Article: PubMed Central - PubMed

Affiliation: Max Planck Institute of Psychiatry Munich, Germany.

ABSTRACT
Comprehensive clinical studies show that adverse conditions in early life can severely impact the developing brain and increase vulnerability to mood disorders later in life. During early postnatal life the brain exhibits high plasticity which allows environmental signals to alter the trajectories of rapidly developing circuits. Adversity in early life is able to shape the experience-dependent maturation of stress-regulating pathways underlying emotional functions and endocrine responses to stress, such as the hypothalamo-pituitary-adrenal (HPA) system, leading to long-lasting altered stress responsivity during adulthood. To date, the study of gene-environment interactions in the human population has been dominated by epidemiology. However, recent research in the neuroscience field is now advancing clinical studies by addressing specifically the mechanisms by which gene-environment interactions can predispose individuals toward psychopathology. To this end, appropriate animal models are being developed in which early environmental factors can be manipulated in a controlled manner. Here we will review recent studies performed with the common aim of understanding the effects of the early environment in shaping brain development and discuss the newly developing role of epigenetic mechanisms in translating early life conditions into long-lasting changes in gene expression underpinning brain functions. Particularly, we argue that epigenetic mechanisms can mediate the gene-environment dialog in early life and give rise to persistent epigenetic programming of adult physiology and dysfunction eventually resulting in disease. Understanding how early life experiences can give rise to lasting epigenetic marks conferring increased risk for mental disorders, how they are maintained and how they could be reversed, is increasingly becoming a focus of modern psychiatry and should pave new guidelines for timely therapeutic interventions.

No MeSH data available.


Related in: MedlinePlus

DNA wraps around histones to form a complex referred to as chromatin. The N-terminal tails of histones serve as sites for epigenetic marking by acetylation and methylation via chromatin remodeling enzymes (e.g., HDACs, HATs, HMTs, and HDMs). DNA methylation refers to the chemical transfer of methyl groups to CpG acceptor sites through a class of enzymes known DNA methyltransferases (DNMTs). Active marks (e.g., histone acetylation and DNA hypomethylation) characterize “open” chromatin, while repressive marks (e.g., histone methylation and DNA hypermethylation) occur at “closed” chromatin.
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Figure 2: DNA wraps around histones to form a complex referred to as chromatin. The N-terminal tails of histones serve as sites for epigenetic marking by acetylation and methylation via chromatin remodeling enzymes (e.g., HDACs, HATs, HMTs, and HDMs). DNA methylation refers to the chemical transfer of methyl groups to CpG acceptor sites through a class of enzymes known DNA methyltransferases (DNMTs). Active marks (e.g., histone acetylation and DNA hypomethylation) characterize “open” chromatin, while repressive marks (e.g., histone methylation and DNA hypermethylation) occur at “closed” chromatin.

Mentions: The epigenome refers to the ensemble of coordinated epigenetic marks that govern accessibility of the DNA to the machinery driving gene expression; inaccessible genes become silenced whereas accessible genes are actively transcribed. Although the understanding of the interplay between epigenetic modifications is still evolving, the modification of core histones that package the DNA into chromatin and methylation of DNA at the cytosine side-chain in cytosine– guanine (CpG) dinucleotides represent the best-understood epigenetic marks (Figure 2).


Epigenetics of early child development.

Murgatroyd C, Spengler D - Front Psychiatry (2011)

DNA wraps around histones to form a complex referred to as chromatin. The N-terminal tails of histones serve as sites for epigenetic marking by acetylation and methylation via chromatin remodeling enzymes (e.g., HDACs, HATs, HMTs, and HDMs). DNA methylation refers to the chemical transfer of methyl groups to CpG acceptor sites through a class of enzymes known DNA methyltransferases (DNMTs). Active marks (e.g., histone acetylation and DNA hypomethylation) characterize “open” chromatin, while repressive marks (e.g., histone methylation and DNA hypermethylation) occur at “closed” chromatin.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3102328&req=5

Figure 2: DNA wraps around histones to form a complex referred to as chromatin. The N-terminal tails of histones serve as sites for epigenetic marking by acetylation and methylation via chromatin remodeling enzymes (e.g., HDACs, HATs, HMTs, and HDMs). DNA methylation refers to the chemical transfer of methyl groups to CpG acceptor sites through a class of enzymes known DNA methyltransferases (DNMTs). Active marks (e.g., histone acetylation and DNA hypomethylation) characterize “open” chromatin, while repressive marks (e.g., histone methylation and DNA hypermethylation) occur at “closed” chromatin.
Mentions: The epigenome refers to the ensemble of coordinated epigenetic marks that govern accessibility of the DNA to the machinery driving gene expression; inaccessible genes become silenced whereas accessible genes are actively transcribed. Although the understanding of the interplay between epigenetic modifications is still evolving, the modification of core histones that package the DNA into chromatin and methylation of DNA at the cytosine side-chain in cytosine– guanine (CpG) dinucleotides represent the best-understood epigenetic marks (Figure 2).

Bottom Line: Here we will review recent studies performed with the common aim of understanding the effects of the early environment in shaping brain development and discuss the newly developing role of epigenetic mechanisms in translating early life conditions into long-lasting changes in gene expression underpinning brain functions.Particularly, we argue that epigenetic mechanisms can mediate the gene-environment dialog in early life and give rise to persistent epigenetic programming of adult physiology and dysfunction eventually resulting in disease.Understanding how early life experiences can give rise to lasting epigenetic marks conferring increased risk for mental disorders, how they are maintained and how they could be reversed, is increasingly becoming a focus of modern psychiatry and should pave new guidelines for timely therapeutic interventions.

View Article: PubMed Central - PubMed

Affiliation: Max Planck Institute of Psychiatry Munich, Germany.

ABSTRACT
Comprehensive clinical studies show that adverse conditions in early life can severely impact the developing brain and increase vulnerability to mood disorders later in life. During early postnatal life the brain exhibits high plasticity which allows environmental signals to alter the trajectories of rapidly developing circuits. Adversity in early life is able to shape the experience-dependent maturation of stress-regulating pathways underlying emotional functions and endocrine responses to stress, such as the hypothalamo-pituitary-adrenal (HPA) system, leading to long-lasting altered stress responsivity during adulthood. To date, the study of gene-environment interactions in the human population has been dominated by epidemiology. However, recent research in the neuroscience field is now advancing clinical studies by addressing specifically the mechanisms by which gene-environment interactions can predispose individuals toward psychopathology. To this end, appropriate animal models are being developed in which early environmental factors can be manipulated in a controlled manner. Here we will review recent studies performed with the common aim of understanding the effects of the early environment in shaping brain development and discuss the newly developing role of epigenetic mechanisms in translating early life conditions into long-lasting changes in gene expression underpinning brain functions. Particularly, we argue that epigenetic mechanisms can mediate the gene-environment dialog in early life and give rise to persistent epigenetic programming of adult physiology and dysfunction eventually resulting in disease. Understanding how early life experiences can give rise to lasting epigenetic marks conferring increased risk for mental disorders, how they are maintained and how they could be reversed, is increasingly becoming a focus of modern psychiatry and should pave new guidelines for timely therapeutic interventions.

No MeSH data available.


Related in: MedlinePlus