Epigenetic mechanisms are key regulators of gene expression, cellular differentiation and development in virtually all tissues including brain. Epigenetic modifications, such as histone modifications and DNA methylation, reflect environmental influences which do not result from alterations in the DNA sequence and represent a central mechanism through which experience can modify brain development, synaptic strength, neural plasticity and neural circuitry. In adulthood, changes in the epigenome are critical to higher cognitive function such as learning and memory.
Emerging evidences implicate dysregulation of epigenetic modifications in neurological disorders and diseases such as brain ischemic stroke, epilepsy, Alzheimer’s, Parkinson’s and Huntington’s disease, neurodevelopmental diseases and psychiatric disorders. Profiling the array of genes that are epigenetically dysregulated in abnormal brain development or neurological disease is likely to advance our understanding of the cognitive impairment and neurodegeneration associated with these disorders and accelerate the identification of novel therapeutic strategies for amelioration of these serious human conditions.
Potential topics include but are not limited to the following aspects or themes associated with the mechanism underlying the pathophysiology of neurological disorders and diseases:
• DNA methylation or hydroxymethylation including regulation of the DNA methyltransferases (DNMTs) and the methylcytosine dioxygenases (TETs)
• Histone modification including regulation of histone acethytransferase, methyltransferase and histone deacetylase
• Histone variants
• Changes in nucleosome positioning
• Non-codingRNA such as microRNAs and long noncoding RNAs
• Transcription regulators that orchestrate epigenetic remodeling of genes such as REST and polycomb proteins
• The epigenetic machinery as a therapeutic target in neurological disorders and diseases – e.g. DNMT or HDAC inhibitors
• The impact of environmental factors such as enriched environment or adverse experience on neuronal fuction and/or plasticiy
Epigenetic mechanisms are key regulators of gene expression, cellular differentiation and development in virtually all tissues including brain. Epigenetic modifications, such as histone modifications and DNA methylation, reflect environmental influences which do not result from alterations in the DNA sequence and represent a central mechanism through which experience can modify brain development, synaptic strength, neural plasticity and neural circuitry. In adulthood, changes in the epigenome are critical to higher cognitive function such as learning and memory.
Emerging evidences implicate dysregulation of epigenetic modifications in neurological disorders and diseases such as brain ischemic stroke, epilepsy, Alzheimer’s, Parkinson’s and Huntington’s disease, neurodevelopmental diseases and psychiatric disorders. Profiling the array of genes that are epigenetically dysregulated in abnormal brain development or neurological disease is likely to advance our understanding of the cognitive impairment and neurodegeneration associated with these disorders and accelerate the identification of novel therapeutic strategies for amelioration of these serious human conditions.
Potential topics include but are not limited to the following aspects or themes associated with the mechanism underlying the pathophysiology of neurological disorders and diseases:
• DNA methylation or hydroxymethylation including regulation of the DNA methyltransferases (DNMTs) and the methylcytosine dioxygenases (TETs)
• Histone modification including regulation of histone acethytransferase, methyltransferase and histone deacetylase
• Histone variants
• Changes in nucleosome positioning
• Non-codingRNA such as microRNAs and long noncoding RNAs
• Transcription regulators that orchestrate epigenetic remodeling of genes such as REST and polycomb proteins
• The epigenetic machinery as a therapeutic target in neurological disorders and diseases – e.g. DNMT or HDAC inhibitors
• The impact of environmental factors such as enriched environment or adverse experience on neuronal fuction and/or plasticiy
