Characterizing Brain and Behavioral Changes in a Mouse Model of Parkinson’s Disease
Location
Science Center: Bent Corridor
Document Type
Poster - Open Access
Start Date
4-28-2023 12:00 PM
End Date
4-28-2023 2:00 PM
Abstract
Parkinson’s Disease (PD) is the second most prevalent neurodegenerative disorder, characterized by the loss of SNc dopamine (DA) neurons, α-Synuclein protein aggregation, and progressive motor deficits. Available treatments for PD patients include DA replacement and other therapies that alleviate motor symptoms. However, these treatments have short-term effectiveness and do not modify disease progression. Additionally, although α-Syn clearance has been extensively researched as a potential target for PD treatment, the origin of α-Syn pathology remains unknown and mounting evidence suggests that α-Syn aggregation may be a symptom of PD, rather than a cause. For instance, heightened oxidative stress, including mitochondrial dysfunction and production of reactive oxygen species, has been implicated in α-Syn aggregation and may initiate the shift toward pathological α-Syn production. However, interventions that ameliorate these upstream pathways are largely underexplored. The goal of this project is to establish a scientific protocol that will allow us to investigate interventions that treat later-stage PD by modifying the underlying mechanisms of PD pathology. To do this, we will first use wild type mice to establish a workflow for assessing motor deficits on the rotarod and in an open field test. We will also demonstrate that we can replicate long-established techniques for characterizing nigrostriatal dopamine cell abundance, including Western blot and immunohistochemistry. Looking ahead, we hope to implement this protocol to characterize neurodegeneration in the MitoPark mouse, a cutting-edge mitochondrial dysfunction model of PD. Our future studies will explore the effect of oxidative stress-targeting treatments on altering disease progression in the MitoPark mouse.
Keywords:
Neurodegeneration, Parkinson's Disease, Mouse model, Mitochondrial damage
Recommended Citation
Lesikar, Brycen; Morehouse, Caroline; and Howard, Christopher, "Characterizing Brain and Behavioral Changes in a Mouse Model of Parkinson’s Disease" (2023). Research Symposium. 21.
https://digitalcommons.oberlin.edu/researchsymp/2023/posters/21
Major
Biology; Neuroscience
Project Mentor(s)
Christopher Howard, Neuroscience
2023
Characterizing Brain and Behavioral Changes in a Mouse Model of Parkinson’s Disease
Science Center: Bent Corridor
Parkinson’s Disease (PD) is the second most prevalent neurodegenerative disorder, characterized by the loss of SNc dopamine (DA) neurons, α-Synuclein protein aggregation, and progressive motor deficits. Available treatments for PD patients include DA replacement and other therapies that alleviate motor symptoms. However, these treatments have short-term effectiveness and do not modify disease progression. Additionally, although α-Syn clearance has been extensively researched as a potential target for PD treatment, the origin of α-Syn pathology remains unknown and mounting evidence suggests that α-Syn aggregation may be a symptom of PD, rather than a cause. For instance, heightened oxidative stress, including mitochondrial dysfunction and production of reactive oxygen species, has been implicated in α-Syn aggregation and may initiate the shift toward pathological α-Syn production. However, interventions that ameliorate these upstream pathways are largely underexplored. The goal of this project is to establish a scientific protocol that will allow us to investigate interventions that treat later-stage PD by modifying the underlying mechanisms of PD pathology. To do this, we will first use wild type mice to establish a workflow for assessing motor deficits on the rotarod and in an open field test. We will also demonstrate that we can replicate long-established techniques for characterizing nigrostriatal dopamine cell abundance, including Western blot and immunohistochemistry. Looking ahead, we hope to implement this protocol to characterize neurodegeneration in the MitoPark mouse, a cutting-edge mitochondrial dysfunction model of PD. Our future studies will explore the effect of oxidative stress-targeting treatments on altering disease progression in the MitoPark mouse.
