Course-Based Research: Examining the Neuroprotective Effects of Caffeine in Multiple Systems Atrophy
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
Multiple Systems Atrophy (MSA) is a neurodegenerative disease characterized by cell shrinkage in areas of the brain involved in motor and body function. Our experiments aim to test the effects of caffeine. the cells based on existing research which suggests that caffeine protects against mutant versions of the ��-synuclein protein (Luan et. al 2018). In MSA oligodendrocytes take in these mutated alpha-synuclein proteins, leading to damaged statutory conduction. We thus experimented on oligodendrocyte-93 cells (OLN-93) introduced to alpha-synuclein proteins to identify if caffeine has potential neuroprotective effects in relation to the MSA phenotype. We experimented on OLN-93 cells exposed to three different types of alpha-synuclein: wild-type, A53E, G51D (the latter two are mutations) and empty plasmid cells as a positive control. Following an initial dose-response curve test we looked at cell viability, mitochondrial function, and free radical production following administration of caffeine. The dose response curve determined that the ideal range of caffeine concentrations for OLN-93 cells for potential neuroprotective effects was between 100-200µM.Using an MTT and Sytox assay we concluded that cell viability increased as the concentration of Caffeine increased. Our analysis additionally concluded that mitochondrial membrane potential increased for the two mutations of ∝-synuclein, while ATP production decreased for all OLN-93 models. In future experiments we will look into the effects of caffeine on oxidative stress and free radical production. So far our data yields promising results for further research on the neuroprotective effects of caffeine on MSA phenotypes.
Keywords:
Neurodegeneration, Caffeine, Multiple Systems Atrophy
Recommended Citation
Peyton, Ava and Wood, Winifred, "Course-Based Research: Examining the Neuroprotective Effects of Caffeine in Multiple Systems Atrophy" (2023). Research Symposium. 8.
https://digitalcommons.oberlin.edu/researchsymp/2023/posters/8
Major
Biology; Neuroscience
Project Mentor(s)
Gunnar Kwakye, Neuroscience
2023
Course-Based Research: Examining the Neuroprotective Effects of Caffeine in Multiple Systems Atrophy
Science Center: Bent Corridor
Multiple Systems Atrophy (MSA) is a neurodegenerative disease characterized by cell shrinkage in areas of the brain involved in motor and body function. Our experiments aim to test the effects of caffeine. the cells based on existing research which suggests that caffeine protects against mutant versions of the ��-synuclein protein (Luan et. al 2018). In MSA oligodendrocytes take in these mutated alpha-synuclein proteins, leading to damaged statutory conduction. We thus experimented on oligodendrocyte-93 cells (OLN-93) introduced to alpha-synuclein proteins to identify if caffeine has potential neuroprotective effects in relation to the MSA phenotype. We experimented on OLN-93 cells exposed to three different types of alpha-synuclein: wild-type, A53E, G51D (the latter two are mutations) and empty plasmid cells as a positive control. Following an initial dose-response curve test we looked at cell viability, mitochondrial function, and free radical production following administration of caffeine. The dose response curve determined that the ideal range of caffeine concentrations for OLN-93 cells for potential neuroprotective effects was between 100-200µM.Using an MTT and Sytox assay we concluded that cell viability increased as the concentration of Caffeine increased. Our analysis additionally concluded that mitochondrial membrane potential increased for the two mutations of ∝-synuclein, while ATP production decreased for all OLN-93 models. In future experiments we will look into the effects of caffeine on oxidative stress and free radical production. So far our data yields promising results for further research on the neuroprotective effects of caffeine on MSA phenotypes.
