Event Title

Gene-Environment Interaction in a Cell Model of Parkinson’s Disease: Alpha-synuclein Modulates Cadmium Transport Dynamics and Homeostasis

Presenter Information

Weelic Chong, Oberlin College

Location

Science Center, A255

Start Date

4-24-2015 4:00 PM

End Date

4-24-2015 5:30 PM

Abtract

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by aggregation of alpha-synuclein (α-syn), whose function is unknown. Perturbations in the function of α-syn and metal homeostasis have been implicated in PD. Our research examines gene-environment interactions between α-syn and acute metal toxicity. Utilizing an established dopaminergic cell model of PD that expresses human wild-type α-syn (N27-syn) or empty vector (N27-vec), I conducted a gene-metal screen to examine α-syn’s neuromodulation of metal-induced toxicity. Our preliminary data explains how an environmental risk factor (cadmium) and a native protein implicated in PD (α-syn) may synergistically interact to cause neurotoxicity and aggravate PD progression.

Notes

Session 3, Panel 18 - Nature vs. Nurture Remixed: Studies in Regulation, Regeneration, Isolation, and Degradation
Moderator: Gunnar Kwakye, Assistant Professor of Neuroscience

Major

Biochemistry; Neuroscience

Advisor(s)

Rebecca Whelan, Chemistry and Biochemistry
Tracie Paine, Neuroscience

Project Mentor(s)

Gunnar Kwakye, Neuroscience

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Apr 24th, 4:00 PM Apr 24th, 5:30 PM

Gene-Environment Interaction in a Cell Model of Parkinson’s Disease: Alpha-synuclein Modulates Cadmium Transport Dynamics and Homeostasis

Science Center, A255

Parkinson’s disease (PD) is a neurodegenerative disorder characterized by aggregation of alpha-synuclein (α-syn), whose function is unknown. Perturbations in the function of α-syn and metal homeostasis have been implicated in PD. Our research examines gene-environment interactions between α-syn and acute metal toxicity. Utilizing an established dopaminergic cell model of PD that expresses human wild-type α-syn (N27-syn) or empty vector (N27-vec), I conducted a gene-metal screen to examine α-syn’s neuromodulation of metal-induced toxicity. Our preliminary data explains how an environmental risk factor (cadmium) and a native protein implicated in PD (α-syn) may synergistically interact to cause neurotoxicity and aggravate PD progression.