School of Science Division of Life Science 31 Investigating Synaptic Transmission in Alzheimer's Disease Supervisor: PARK Hyo Keun / LIFS Student: LEE Kayeon / BCB Course: UROP 1000, Summer As the population is aging worldwide, the incidence of Alzheimer’s disease is also on the rise. Even though biomedical knowledge has been developing rapidly, in Alzheimer’s disease There are still many unknowns, such as the exact cause of the disease and the mechanism of aggregated proteins. Among various causes of the disease, the relation with Tau protein has been brought up recently. This project will explore about the synaptic transmission difference between Tau P301L mutant and wild type on Alzheimer’s disease. By imaging vesicle transmission in mouse neurons with FM4-64 dye, exocytosis of synaptic vesicles will be explored. The data of imaging can be analyzed by checking fluorescence intensity change. The loss of fluorescence indicates that vesicle activity was robust. Investigating Synaptic Transmission in Alzheimer's Disease Supervisor: PARK Hyo Keun / LIFS Student: LO Wai Yan / BCB Course: UROP 1100, Fall Alzheimer’s disease (AD) is one of the most prevalent neurodegenerative disorders, affecting millions of individuals worldwide. Characterized by synaptic dysfunction and neurodegeneration, AD is increasingly recognized for the central role of tau pathology in its progression. This research project aimed to investigate the impact of tau phosphorylation in synaptic transmission in Alzheimer’s disease. However, this project remains unfinished. Thus, this project will solely focus on the differences in synaptic transmission with excitatory pre-synapse markers for tau t217-wild type brain cell, which showed linkage to cognitive impairments observed in Alzheimer disease’s model, tau t217-non-phospho-mimic (T217A), which is expected to give no exacerbation in cognitive impairments and tau t217-phospho-mimic (T217E), which mimics the phosphorylated state in tau t217-wild-type. As the result, tau t217-wild type and T217E brain cell should show a weaker excitatory neurotransmission ability than tau t217-non-phospho-mimic (T217A). Investigating Synaptic Transmission in Alzheimer's Disease Supervisor: PARK Hyo Keun / LIFS Student: SUNG Hyun / BIOT-AB Course: UROP 1000, Summer Synaptic dysfunction is a significant feature of Alzheimer’s disease, yet the mechanisms underlying impaired synaptic vesicle exocytosis remain unclear. To investigate the effect of pathological tau on synaptic transmission, rat hippocampal neurons were transfected with either Wild Type (WT) or P301L tau proteins fused to GFP using lipofectamine. Synaptic vesicle release was visualized through FM 1-43 and FM 4-64 dye imaging to compare exocytosis dynamics between WT and P301L tau-expressing neurons. The results demonstrate that neurons expressing P301L tau exhibit significantly reduced synaptic vesicle exocytosis compared to WT controls, suggesting that tau pathology associated with Alzheimer’s disease directly impairs neurotransmitter release. These findings provide insights into the synaptic deficits of Alzheimer’s disease.
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