Induction of Alpha-Synuclein Pathology in the ENS of the Rat and Non-Human Primates Results in Gastointestinal Dymotility and Transient CNS Pathology
Location
Hager-Lubbers Exhibition Hall
Description
PURPOSE: The purpose of this study is to determine whether alpha-synuclein (a-syn) pathology can be initiated in the enteric nervous system (ENS) and spread to the central nervous system (CNS) over time. A-syn is a major protein involved in familial and sporadic Parkinson’s disease (PD); PD is a progressive neurodegenerative disorder, the cause of which remains unknown. The ENS is important to study for two reasons: first, the most significant clinical presentations of PD is gastric dysfunction, and second, accumulation of Lewy bodies (primarily a-syn aggregates) can be found in ENS myenteric and submucosal neurons. CHALLENGE: Although aggregated a-syn has been shown to cause conversion of functional a-syn to insoluble proteins, how a-syn becomes toxic to the neurons and relates to the pathophysiology of PD is unknown. EXPERIENCE: I had worked independently on several assigned tasks such as brain dissection and its sample collection and staining, as well as working as part of the research team. OUTCOME: The outcome of this project implied that the spread of a-syn pathology from enteric neurons to the CNS is limited and not adequate to sustain pathological spread of a-syn throughout the CNS on its own. IMPACT: I had gained many technical and professional skills during my one-year internship. It also helped me better understand a research lab dynamic. The challenges I had while performing certain task or repeating protocols helped me to adapt to become a better scientist. I was hired as a research technician to continue the research after my internship.
Induction of Alpha-Synuclein Pathology in the ENS of the Rat and Non-Human Primates Results in Gastointestinal Dymotility and Transient CNS Pathology
Hager-Lubbers Exhibition Hall
PURPOSE: The purpose of this study is to determine whether alpha-synuclein (a-syn) pathology can be initiated in the enteric nervous system (ENS) and spread to the central nervous system (CNS) over time. A-syn is a major protein involved in familial and sporadic Parkinson’s disease (PD); PD is a progressive neurodegenerative disorder, the cause of which remains unknown. The ENS is important to study for two reasons: first, the most significant clinical presentations of PD is gastric dysfunction, and second, accumulation of Lewy bodies (primarily a-syn aggregates) can be found in ENS myenteric and submucosal neurons. CHALLENGE: Although aggregated a-syn has been shown to cause conversion of functional a-syn to insoluble proteins, how a-syn becomes toxic to the neurons and relates to the pathophysiology of PD is unknown. EXPERIENCE: I had worked independently on several assigned tasks such as brain dissection and its sample collection and staining, as well as working as part of the research team. OUTCOME: The outcome of this project implied that the spread of a-syn pathology from enteric neurons to the CNS is limited and not adequate to sustain pathological spread of a-syn throughout the CNS on its own. IMPACT: I had gained many technical and professional skills during my one-year internship. It also helped me better understand a research lab dynamic. The challenges I had while performing certain task or repeating protocols helped me to adapt to become a better scientist. I was hired as a research technician to continue the research after my internship.