Dr Jordan Wright
Dr Jordan Wright
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Research overview
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID), seizures, mobility issues and autistic behaviours.
Over the past decade, clinical genetics has been able to solve the genetic causes of some NDDs, linking them to >1000 genes thus far, of which >70 result from deleterious mutations within epigenetic regulatory genes – referred to as epigenetic NDDs. These genes encode proteins that place modifications on DNA and histones (which wrap and compact DNA into 'chromatin'), and it is these modifications that determine if genes are 'switched on' (expressed) or 'switched off' (silenced). Histone modifications can be altered by specialised proteins and it is the balance between adding and removing histone modifications that allows timely, coordinated regulation of gene expression. In epigenetic NDDs, this process is dysregulated, histone modification is reduced and severe neurodevelopmental outcomes result.
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID), seizures, mobility issues and autistic behaviours.
Over the past decade, clinical genetics has been able to solve the genetic causes of some NDDs, linking them to >1000 genes thus far, of which >70 result from deleterious mutations within epigenetic regulatory genes – referred to as epigenetic NDDs. These genes encode proteins that place modifications on DNA and histones (which wrap and compact DNA into 'chromatin'), and it is these modifications that determine if genes are 'switched on' (expressed) or 'switched off' (silenced). Histone modifications can be altered by specialised proteins and it is the balance between adding and removing histone modifications that allows timely, coordinated regulation of gene expression. In epigenetic NDDs, this process is dysregulated, histone modification is reduced and severe neurodevelopmental outcomes result.
Research overview
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID),...
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID),...
Research overview
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID), seizures, mobility issues and autistic behaviours.
Over the past decade, clinical genetics has been able to solve the genetic causes of some NDDs, linking them to >1000 genes thus far, of which >70 result from deleterious mutations within epigenetic regulatory genes – referred to as epigenetic NDDs. These genes encode proteins that place modifications on DNA and histones (which wrap and compact DNA into 'chromatin'), and it is these modifications that determine if genes are 'switched on' (expressed) or 'switched off' (silenced). Histone modifications can be altered by specialised proteins and it is the balance between adding and removing histone modifications that allows timely, coordinated regulation of gene expression. In epigenetic NDDs, this process is dysregulated, histone modification is reduced and severe neurodevelopmental outcomes result.
NeuroDevelopmental Disorders (NDDs) are a group of conditions characterised by abnormal development and function of the central nervous system. They result in a range of neurological symptoms including intellectual disability (ID), seizures, mobility issues and autistic behaviours.
Over the past decade, clinical genetics has been able to solve the genetic causes of some NDDs, linking them to >1000 genes thus far, of which >70 result from deleterious mutations within epigenetic regulatory genes – referred to as epigenetic NDDs. These genes encode proteins that place modifications on DNA and histones (which wrap and compact DNA into 'chromatin'), and it is these modifications that determine if genes are 'switched on' (expressed) or 'switched off' (silenced). Histone modifications can be altered by specialised proteins and it is the balance between adding and removing histone modifications that allows timely, coordinated regulation of gene expression. In epigenetic NDDs, this process is dysregulated, histone modification is reduced and severe neurodevelopmental outcomes result.
Top Publications
- Ermine, CM, Wright, JL, Stanic, D, Parish, CL, Thompson, LH. Ischemic Injury Does Not Stimulate Striatal Neuron Replacement Even during Periods of Active Striatal Neurogenesis.. iScience 23(6) : 101175 2020 view publication
- Wright, JL, Chu, HX, Kagan, BJ, Ermine, CM, Kauhausen, JA, Parish, CL, Sobey, CG, Thompson, LH. Local Injection of Endothelin-1 in the Early Neonatal Rat Brain Models Ischemic Damage Associated with Motor Impairment and Diffuse Loss in Brain Volume.. Neuroscience 393: 110 -122 2018 view publication
- Ermine, CM, Wright, JL, Frausin, S, Kauhausen, JA, Parish, CL, Stanic, D, Thompson, LH. Modelling the dopamine and noradrenergic cell loss that occurs in Parkinson's disease and the impact on hippocampal neurogenesis.. Hippocampus 28(5) : 327 -337 2018 view publication
- Xiao, L, Ohayon, D, McKenzie, IA, Sinclair-Wilson, A, Wright, JL, Fudge, AD, Emery, B, Li, H, Richardson, WD. Rapid production of new oligodendrocytes is required in the earliest stages of motor-skill learning.. Nat Neurosci 19(9) : 1210 -1217 2016 view publication
- Wright, JL, Ermine, CM, Jørgensen, JR, Parish, CL, Thompson, LH. Over-Expression of Meteorin Drives Gliogenesis Following Striatal Injury.. Front Cell Neurosci 10: 177 2016 view publication
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