Charlotte Russell
Research Mentor: Wei-Chih Chang
Mentor Department: Molecular and Integrative Physiology, Medicine
Author(s): Charlotte Russell, Geoffrey Murphy, Wei-Chih Chang
Session: Session 5 (2:00 PM – 2:50 PM)
Presentation Type: Poster 127
Abstract
Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by dementia and intellectual impairment. The brains of AD patients have been found to feature ß-amyloid (Aß) plaques, indicating that Aß is the cause of AD. However, recent clinical trials that have interfered with the build-up of Aß within the brain were not successful in reversing or even slowing down the functional deteriorations associated with AD. This suggests that Aß has multifaceted, early-onset, and long-lasting impacts on the brain that are mostly unknown. In the pursuit of further understanding Aß’s impacts and promoting development in preventing and aiding with AD symptoms, I studied ex vivo spontaneous neuronal network activity with or without Aß. Hippocampal slices (400 µm) were prepared from normal aging mice and a mouse AD model (5xFAD); Aß (500 nM) was applied to the slices after acquiring the basal network activity induced by high potassium (8 mM) artificial cerebrospinal fluid. I found that without Aß, network activity initiated from the hippocampus or the cortex, equivalently, and both kinds of activity spread to the other region. Aß attenuated the hippocampus-driven activity and disrupted the transmission from the cortex. The results suggest the vulnerability of the hippocampus and the initial mechanism underlying AD-related memory loss.
