About this Research Topic
The dynamic and finely tuned regulation of gene expression is key in specifying cellular identity by adding another layer of complexity and regulation that ensures proper Central Nervous System (CNS) development.
Experience-dependent neuronal plasticity allows organisms to adapt and respond to changes in the environment. Neuronal plasticity includes sustained modifications in synaptic structure and function that require de novo gene expression. The regulation of gene expression is a critical molecular mechanism mediating stable adaptations and maladaptation in the brain. Indeed, neuropsychiatric disorders are characterized by disruptions in the transcription regulation in various brain areas, and this is represented also in different preclinical and in vitro models of such disorders. For instance, aberrant histone modifications were studied in model organisms and patients with neuropsychiatric disorders, such as major depression, bipolar disorder, and schizophrenia. Therefore, several model organisms (e.g. rodents, non-human primates), including invertebrate Drosophila melanogaster, have been developed to better stratify the mechanisms and molecular pathways involved in these epigenetically driven diseases.
The study of the epigenetic landscape in CNS diseases has recently advanced, with a focus on the identification of the epigenetic signatures involved in brain disease. Any imbalances in epigenetic regulation of gene transcription such as histone/DNA modifications, as well as expression of various forms of non-coding RNAs (e.g. miRNAs, piRNAs, siRNA, and lncRNA) may lead to aberrant outcomes at multi-layer levels (e.g., molecular, cellular, circuit, and behavior), leading to the pathogenesis and pathophysiology of neuropsychiatric disorders. Furthermore, increasing evidence suggests that epigenetic drugs, such as HDAC and DNMT inhibitors, are effective for selective neuropsychiatric disorders.
Additionally, there has been recent interest in the possibility that epigenetic mechanisms might contribute to the transgenerational transmission of disease risk and resilience. This research is important for understanding the factors that influence risk for neuropsychiatric disorders, such as depression, anxiety, and autism, and may have the potential to contribute to the development of innovative treatments that can more precisely target vulnerable populations.
Despite the current advancement in understanding chromatin biology through several advanced methodologies, the impact of deregulated epigenetic control on CNS development (glial/neuronal), function, behavior, neuropsychiatric disorders, as well as the transgenerational influence of epigenetic changes is still poorly understood.
We intend to collect novel studies, reviews, methodological papers (in vivo, in vitro) using several model organisms for a comprehensive perspective on the role of the epigenome in neuropsychiatric disorders.
The following subtopics are welcome:
● Crosstalk between histone and DNA modifications in neuropsychiatric disorders
● DNA methylation/demethylation both during development and in adulthood and its role in gene regulation affecting behavior in mammals and invertebrate models such as Drosophila melanogaster
● The role of non-coding RNAs in neurodevelopmental and psychiatric disorders
● The role of retrotransposons in neurodevelopmental and psychiatric disorders
● Molecular mechanisms underlying changes in the epigenome of the CNS
● Molecular and cellular mechanisms of therapeutic drugs for psychiatric disorders (e.g., antidepressants and antipsychotics)
● The role of epigenetics in cellular and behavioral heterogeneity (or individual differences)
● Epigenetic pharmacotherapy (e.g., HDAC inhibitor, dCas9 fused to the catalytic domain of an epigenetic enzyme) on neuronal and behavioral dysfunction. An epigenetic, transgenerational model of psychiatric disorders
Experience-dependent neuronal plasticity allows organisms to adapt and respond to changes in the environment. Neuronal plasticity includes sustained modifications in synaptic structure and function that require de novo gene expression. The regulation of gene expression is a critical molecular mechanism mediating stable adaptations and maladaptation in the brain. Indeed, neuropsychiatric disorders are characterized by disruptions in the transcription regulation in various brain areas, and this is represented also in different preclinical and in vitro models of such disorders. For instance, aberrant histone modifications were studied in model organisms and patients with neuropsychiatric disorders, such as major depression, bipolar disorder, and schizophrenia. Therefore, several model organisms (e.g. rodents, non-human primates), including invertebrate Drosophila melanogaster, have been developed to better stratify the mechanisms and molecular pathways involved in these epigenetically driven diseases.
The study of the epigenetic landscape in CNS diseases has recently advanced, with a focus on the identification of the epigenetic signatures involved in brain disease. Any imbalances in epigenetic regulation of gene transcription such as histone/DNA modifications, as well as expression of various forms of non-coding RNAs (e.g. miRNAs, piRNAs, siRNA, and lncRNA) may lead to aberrant outcomes at multi-layer levels (e.g., molecular, cellular, circuit, and behavior), leading to the pathogenesis and pathophysiology of neuropsychiatric disorders. Furthermore, increasing evidence suggests that epigenetic drugs, such as HDAC and DNMT inhibitors, are effective for selective neuropsychiatric disorders.
Additionally, there has been recent interest in the possibility that epigenetic mechanisms might contribute to the transgenerational transmission of disease risk and resilience. This research is important for understanding the factors that influence risk for neuropsychiatric disorders, such as depression, anxiety, and autism, and may have the potential to contribute to the development of innovative treatments that can more precisely target vulnerable populations.
Despite the current advancement in understanding chromatin biology through several advanced methodologies, the impact of deregulated epigenetic control on CNS development (glial/neuronal), function, behavior, neuropsychiatric disorders, as well as the transgenerational influence of epigenetic changes is still poorly understood.
We intend to collect novel studies, reviews, methodological papers (in vivo, in vitro) using several model organisms for a comprehensive perspective on the role of the epigenome in neuropsychiatric disorders.
The following subtopics are welcome:
● Crosstalk between histone and DNA modifications in neuropsychiatric disorders
● DNA methylation/demethylation both during development and in adulthood and its role in gene regulation affecting behavior in mammals and invertebrate models such as Drosophila melanogaster
● The role of non-coding RNAs in neurodevelopmental and psychiatric disorders
● The role of retrotransposons in neurodevelopmental and psychiatric disorders
● Molecular mechanisms underlying changes in the epigenome of the CNS
● Molecular and cellular mechanisms of therapeutic drugs for psychiatric disorders (e.g., antidepressants and antipsychotics)
● The role of epigenetics in cellular and behavioral heterogeneity (or individual differences)
● Epigenetic pharmacotherapy (e.g., HDAC inhibitor, dCas9 fused to the catalytic domain of an epigenetic enzyme) on neuronal and behavioral dysfunction. An epigenetic, transgenerational model of psychiatric disorders
Keywords: Epigenetics, Histone Modifications, DNA/RNA Modifications, Model Organisms, Central Nervous System, Neurodevelopment, Neuropsychiatric Disorders, Mental Health, Clinical Data, Transgenerational
Important Note: All contributions to this Research Topic must be within the scope of the section and journal to which they are submitted, as defined in their mission statements. Frontiers reserves the right to guide an out-of-scope manuscript to a more suitable section or journal at any stage of peer review.
