37th Annual Student Research Conference
Correlating Cellular Changes with Amyloid Plaque Size in a Genetic Alzheimer’s Disease Model
Katelyn N. Chimienti
Dr. Stephanie Maiden, Faculty Mentor
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss, deteriorated thinking skills, and the eventual inability to perform simple tasks. Cellularly, AD is associated with neuronal loss and brain inflammation, caused by accumulation of amyloid-? and hyperphosphorylated tau proteins. The aim of my study is to analyze cellular changes associated with amyloid-? plaques in brains of mice overexpressing human amyloid precursor protein and presenilin-1 (APP/PS1). One-year-old APP/PS1 transgenic mice were perfused with paraformaldehyde, brains were dissected, and cut into 30 µm sections using a vibratome. Forebrain sections were stained with fluorescently-labeled antibodies for cell markers (NeuN = neurons; IBA1 = microglia; GFAP = astrocytes; synaptophysin = presynaptic vesicle; vGlut2 = glutamate transporter). Amyloid plaques were identified by staining with amyloid dye X-34 staining. Changes in the different cellular markers will be compared between the early stage of plaques (small size) vs a progressed stage of plaques (large plaques).
Keywords: Alzheimer's Disease, Amyloid beta plaques , tau proteins , APP/PS1, cellular markers
Topic(s):Biology
Presentation Type: Poster Presentation
Session: 3-2
Location: SUB Activities Room
Time: 3:15