Juliana Alicja Zink Pedersen

Scientific focus areas:

• In vitro disease modelling using human induced pluripotent stem cells (hiPSC)

• Differentiation of hiPSCs to dopaminergic neurons and mature astrocytes

• Neuron-astrocyte co-culture

• Intercellular organelle and α-synuclein transfer, including mitochondrial transfer Bioimaging (live cell bioimaging and ICC)​

 

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Current project:

Neuron-astrocyte interactions in Parkinson’s disease: mechanisms of intercellular organelle and α-synuclein transfer

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Project description:

Parkinson’s disease (PD) is the second most prevalent and fastest growing neurodegenerative disorder. Degeneration of dopaminergic neurons in substantia nigra pars compacta (SNpc) and a-synuclein accumulation are both pathological hallmarks of PD (1,2). Recent studies suggest that mitochondria can be transferred intercellularly between astrocytes and neurons (3,4). Furthermore, glia-glia and glia-neuron intercellular transfer of a-synuclein has been reported (5,6). Further investigation of the mechanisms of organelle transfer could reveal potential therapeutic targets for enhancing transfer of functional mitochondria or preventing the spread of a-synuclein pathology.
This Ph.D. project explores the role of neuron-astrocyte interactions in PARK2-mediated Parkinson’s disease (PD) using human induced pluripotent stem cells (hiPSCs). The focus of this project is to investigate the mechanisms of intercellular organelle and a-synuclein transfer. The hypothesis of this project is that astrocyte-mediated intercellular transfer of functional mitochondria can rescue PARK2-KO dopaminergic neurons, and moreover that mitochondrial and lysosomal dysfunction in neuron-astrocyte interactions lead to a-synuclein accumulation and subsequent degeneration of dopaminergic neurons in PD.