39th Annual Student Research Conference
Amyloid plaque size correlates with cellular changes in a genetic Alzheimer's disease model
Whitney A. Pavely* and Aiden Moriarty
Dr. Stephanie Maiden, Dr. Daniela Ostrowski (A.T. Still University), Dr. Tim Ostrowski (A.T. Still University), and Dr. Byunghee Han (A.T. Still University), Faculty Mentors
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by memory loss and the inability to perform simple tasks. AD is associated with neuronal loss and inflammation caused by accumulation of amyloid-? and hyperphosphorylated tau proteins. Our study aims 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 and brains were cut into 30 µm sections. Forebrain sections were stained with fluorescently-labeled antibodies for various cell markers (NeuN = neurons; IBA1 = microglia; GFAP = astrocytes; synaptophysin = presynaptic vesicle; GAD67 = glutamic acid decarboxylase 67 kDa; vGlut2 = glutamate transporter; EAAT2 = excitatory amino acid transporter 2). 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 (large plaques).
Keywords: Alzheimer's Disease, amyloid-β, cell markers
Topic(s):Biology
Presentation Type: Oral Presentation
Session: -4
Location: MG 1000
Time: 1:45