Michael Dew (mpd197@student.byu.edu)

Since its initial elucidation nearly 100 years ago, Alzheimer's disease has been associated with sharp declines in cognitive abilities ranging from memory recall and formation to rational thought. While the exact mechanism behind Alzheimer-induced dementia remains an area of active research, there is clear evidence of its deleterious effects on synaptic health and plasticity (Alzheimer's Association 2022). Synaptic plasticity refers to the ability of neurons to create or destroy synaptic connections. Creating and strengthening neural connections is mediated through the process of Long Term Potentiation (LTP) while weakening or breaking synaptic connections is thought to be mediated through the process of Long Term Depotentiation (LTD). Consequently, LTP has been associated with learning and LTD with forgetting. The exact mechanism for both processes remain unclear, but current data suggests that the metabotropic glutamate receptor 5 (mGluR5) plays an important role in the physiological basis of LTD and, by extension, forgetting (Gladding et al., 2009). This mechanism has been studied in male models but has yet to be characterized in female models; consequently, we intend to replicate recent studies with the modification of characterizing male and female models of mGluR5-induced LTD.