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Support Cells and Dopaminergic Neurons

Brain iron increases significantly during ageing and is even further elevated in Parkinson’s disease. The death of dopaminergic neurons contributes to motor deficits characteristic of this disease. While iron is essential for normal function of these neurons, increased levels within these cells may be a trigger a newly identified form of cell death that drives neurodegeneration. The health of dopaminergic neurons is also supported by closely associated glial cells. However, the details of how glial dysfunction affects dopaminergic cell viability need further examination.

Aims

To use Caenorhabditis elegans, a model organism with powerful genetics, to understand how losing control of iron homeostasis in glial cells contributes to the loss of dopaminergic neurons.

  • Using transgenic manipulation of iron homeostasis and dopamine.
  • Model dopaminergic cell loss through cell specific (including glia) genetic manipulations

We will explore early life changes to the dopaminergic system through to neuronal death in late life. Understanding how the interactions between iron, glia and dopamine change through lifespan will provide new avenues for interventions to prevent cell death in Parkinson’s disease.

Figure: Cephalic sheath glia in C. elegans: CEPsh cells (Blue), CEP dopaminergic neurons (Pink), Nerve ring (Red)

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