Presenters: Jed Christensen
Authors: Jeffrey Edwards, Jed Christensen, Michael Dew, Cami Staker
Faculty Advisor: Jeffrey Edwards
Institution: Brigham Young University
Neurodegenerative diseases such as Alzheimer’s are increasingly prevalent worldwide. Understanding the mechanisms of neurodegeneration is essential to finding treatments and preventions for the effects of these diseases. Degeneration in Alzheimer’s has been linked to synaptic plasticity, including a decrease in the process of synaptic strengthening, which is long-term potentiation (LTP), and/or an increase in the process of synaptic weakening, which is depotentiation (1). While recording from the hippocampus, the memory center of the brain, we will first induce LTP and then depotentiate this plasticity. We propose a metabotropic glutamate receptor (mGluR5) is involved in this phenomenon. We plan to use electrophysiology experiments to measure this depotentiation effect. We will perform experiments both alone and in the presence of an mGluR5 antagonist to identify the potential mechanisms of inducing depotentiation through mGluR5 receptors. Results from our study will indicate how mGluR5 receptors are involved in synaptic plasticity, specifically depotentiation. Understanding the role of mGluR5 could indicate pathways that could be targeted by preventive medicine or practices in order to decrease the risk of developing the disease. 1.Li, S., & Selkoe, D. J. (2020). A mechanistic hypothesis for the impairment of synaptic plasticity by soluble AΒ oligomers from alzheimer’s brain.Journal of Neurochemistry,154(6), 583–597. https://doi.org/10.1111/jnc.15007 [https://doi.org/10.1111/jnc.15007]