Systems biology of complex symptom profiles: Capturing interactivity across behavior, brain and immune regulation

Broderick, Gordon; Craddock, Travis J. A.

doi:10.1016/j.bbi.2012.09.008

Cited by 21 publications

(18 citation statements)

References 60 publications

(70 reference statements)

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“…Unbridled stable homeostasis would generate a brain that could respond quickly to existing routines and information, but respond poorly to novelty or insult. Whether plasticity will be adaptive or maladaptive depends on homeostatic regulation, which exists at the level of gene, transcript, protein, metabolite, cell, and brain (Broderick & Craddock, 2012). …”

Section: Plastic Change Operates In Concert With Homeostatic Mechamentioning

confidence: 99%

Age, plasticity, and homeostasis in childhood brain disorders

Dennis¹,

Spiegler²,

Juranek³

et al. 2013

Neuroscience & Biobehavioral Reviews

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It has been widely accepted that the younger the age and/or immaturity of the organism, the greater the brain plasticity, the young age plasticity privilege. This paper examines the relation of a young age to plasticity, reviewing human pediatric brain disorders, as well as selected animal models, human developmental and adult brain disorder studies. As well, we review developmental and childhood acquired disorders that involve a failure of regulatory homeostasis. Our core arguments are: Plasticity is neutral with respect to outcome. Although the effects of plasticity are often beneficial, the outcome of plasticity may be adaptive or maladaptive.The young age plasticity privilege has been overstated.Plastic change operates in concert with homeostatic mechanisms regulating change at every point in the lifespan.The same mechanisms that propel developmental change expose the immature brain to adverse events, making it more difficult for the immature than for the mature brain to sustain equilibrium between plasticity and homeostasis.Poor outcome in many neurodevelopmental disorders and childhood acquired brain insults is related to disequilibrium between plasticity and homeostasis.

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Section: Plastic Change Operates In Concert With Homeostatic Mechamentioning

confidence: 99%

Age, plasticity, and homeostasis in childhood brain disorders

Dennis¹,

Spiegler²,

Juranek³

et al. 2013

Neuroscience & Biobehavioral Reviews

View full text Add to dashboard Cite

show abstract

“…The data will also provide a valuable method to identify epigenetically invariant genomic regions that can serve to reduce genomic complexity in genome-wide analysis of epigenetic signaling, and transcriptional “silent” regions in specified cell types unlikely to be responsive to environmental perturbations. These data, together with an accumulating array of published epigenomic analysis, should help move research on the impacts of early life adversity beyond candidate gene to “candidate pathway” and “candidate network” levels of analysis, which are finding utility in other areas of complex disease research [e.g., (38)].…”

Section: Epigenomic Regulation By Early Life Adversity In Gene Regulamentioning

confidence: 99%

Epigenomic Mechanisms of Early Adversity and HPA Dysfunction: Considerations for PTSD Research

McGowan¹

2013

Front. Psychiatry

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Childhood adversity can have life-long consequences for the response to stressful events later in life. Abuse or severe neglect are well-known risk factors for post-traumatic stress disorder (PTSD), at least in part via changes in neural systems mediating the endocrine response to stress. Determining the biological signatures of risk for stress-related mental disorders such as PTSD is important for identifying homogenous subgroups and improving treatment options. This review will focus on epigenetic regulation in early life by adversity and parental care – prime mediators of offspring neurodevelopment – in order to address several questions: (1) what have studies of humans and analogous animal models taught us about molecular mechanisms underlying changes in stress-sensitive physiological systems in response to early life trauma? (2) What are the considerations for studies relating early adversity and PTSD risk, going forward? I will summarize studies in animals and humans that address the epigenetic response to early adversity in the brain and in peripheral tissues. In so doing, I will describe work on the glucocorticoid receptor and other well-characterized genes within the stress response pathway and then turn to genomic studies to illustrate the use of increasingly powerful high-throughput approaches to the study of epigenomic mechanisms.

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“…The data will also provide a valuable method to identify epigenetically invariant genomic regions that can serve to reduce genomic complexity in genomewide analysis of epigenetic signaling, and transcriptional "silent" regions in specified cell types unlikely to be responsive to environmental perturbations. These data, together with an accumulating array of published epigenomic analysis, should help move research on the impacts of early life adversity beyond candidate gene to "candidate pathway" and "candidate network" levels of analysis, which are finding utility in other areas of complex disease research [e.g., (38)]. …”

Section: Epigenomic Regulation By Early Life Adversity In Gene Regulamentioning

confidence: 99%

Suicidal Behaviors Among Adolescents in Juvenile Detention: Role of Adverse Life Experiences

2015

The Societal Burden of Child Abuse

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Childhood adversity can have life-long consequences for the response to stressful events later in life. Abuse or severe neglect are well-known risk factors for post-traumatic stress disorder (PTSD), at least in part via changes in neural systems mediating the endocrine response to stress. Determining the biological signatures of risk for stress-related mental disorders such as PTSD is important for identifying homogenous subgroups and improving treatment options. This review will focus on epigenetic regulation in early life by adversity and parental care -prime mediators of offspring neurodevelopment -in order to address several questions: (1) what have studies of humans and analogous animal models taught us about molecular mechanisms underlying changes in stress-sensitive physiological systems in response to early life trauma? (2) What are the considerations for studies relating early adversity and PTSD risk, going forward? I will summarize studies in animals and humans that address the epigenetic response to early adversity in the brain and in peripheral tissues. In so doing, I will describe work on the glucocorticoid receptor and other well-characterized genes within the stress response pathway and then turn to genomic studies to illustrate the use of increasingly powerful high-throughput approaches to the study of epigenomic mechanisms.

show abstract

Systems biology of complex symptom profiles: Capturing interactivity across behavior, brain and immune regulation

Cited by 21 publications

References 60 publications

Age, plasticity, and homeostasis in childhood brain disorders

Age, plasticity, and homeostasis in childhood brain disorders

Epigenomic Mechanisms of Early Adversity and HPA Dysfunction: Considerations for PTSD Research

Suicidal Behaviors Among Adolescents in Juvenile Detention: Role of Adverse Life Experiences

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