Session 2G: Characterization of Alzheimer's Disease Associated Amyloid Beta Oligomers and Phosphorylated Tau in the Developing Avian CNS
Session Number
Session 2G: 1st Presentation
Advisor(s)
Drs. Kirsten Viola and Dr. William Klein, Northwestern University
Location
Room A115
Start Date
26-4-2018 10:35 AM
End Date
26-4-2018 11:20 AM
Abstract
Animal models have been instrumental in studying the progression, pathology, and symptomology of diseases, and are thus essential to our current understanding of diseases. One particular disease of interest today, Alzheimer's disease {AD), also uses these animal models. It is now accepted that Amyloid Beta oligomers (APOs), soluble derivative aggregates of the Amyloid Beta precursor protein (APP), are responsible for the pathology and neurotoxicity of AD through tau hyperphosphorylation, synaptic deregulation, and reactive oxidative damage. Previous results have demonstrated that phosphorylated tau protein is present in the developing chick brain but drop off in concentration once maturity is reached (Pope, et al. 1993). Our study investigated the roles of APOs and phosphorylated tau protein in central nervous system development, using chick embryos as our animal model due to the almost identical epitopes of APP and tau protein in the avian and human central nervous systems. This research has important therapeutic uses as investigating the role of these proteins in development gives valuable insight into the mechanisms of neurotoxicity and synaptic loss in AD, opening pathways for new treatment methods and early identification protocols.
Session 2G: Characterization of Alzheimer's Disease Associated Amyloid Beta Oligomers and Phosphorylated Tau in the Developing Avian CNS
Room A115
Animal models have been instrumental in studying the progression, pathology, and symptomology of diseases, and are thus essential to our current understanding of diseases. One particular disease of interest today, Alzheimer's disease {AD), also uses these animal models. It is now accepted that Amyloid Beta oligomers (APOs), soluble derivative aggregates of the Amyloid Beta precursor protein (APP), are responsible for the pathology and neurotoxicity of AD through tau hyperphosphorylation, synaptic deregulation, and reactive oxidative damage. Previous results have demonstrated that phosphorylated tau protein is present in the developing chick brain but drop off in concentration once maturity is reached (Pope, et al. 1993). Our study investigated the roles of APOs and phosphorylated tau protein in central nervous system development, using chick embryos as our animal model due to the almost identical epitopes of APP and tau protein in the avian and human central nervous systems. This research has important therapeutic uses as investigating the role of these proteins in development gives valuable insight into the mechanisms of neurotoxicity and synaptic loss in AD, opening pathways for new treatment methods and early identification protocols.