Session Number
Session 2E: 1st Presentation
Advisor(s)
Kirsten Viola, Northwestern University
Location
Room A113
Start Date
28-4-2017 10:00 AM
End Date
28-4-2017 11:15 AM
Abstract
One of the greatest advancements in Alzheimer's disease (AD) diagnostics has been the implementation of positron emission tomography (PET) probes that target amyloid fibrils and plaques. However, these protein congregations do not correlate closely to the pathogenesis of AD. It is now believed that amyloid-beta oligomers (ABOs) appear in the earliest stages of AD cause memory dysfucntion through tau hyperphosphorylation, oxidative damage, and synaptic loss. Due to the inability to reverse neuronal loss, it is critical that diagnostic probes with the ability to target biomarkers that appear years before the onset of neurodegeneration. Because ABOs are considered the first toxin to appear in AD pathogenesis and thus are an excellent candidate for an early diagnostic imaging probe, we developed antibodytargeted, ABO specific PET probes using the mouse NU4 and human ACU193 antibodies. The development of such probes will allow for the early identification of those who demonstrate AD pathology, but still lack memory deficits, which would allow for the implementation of preventative measures, precise correlation of ABO buildup with the development of memory loss, tau hyperphosporylation, and the identification of therapeutics. Evidence presented here showcases the tremendous potential of NU4PET and ACU193PET as a novel diagnostic agent for AD.
Session 2E: The Development of a Humanized Antibody-Targeted AβO-Specific PET Probe for Early Diagnostic Imaging of Alzheimer's Disease
Room A113
One of the greatest advancements in Alzheimer's disease (AD) diagnostics has been the implementation of positron emission tomography (PET) probes that target amyloid fibrils and plaques. However, these protein congregations do not correlate closely to the pathogenesis of AD. It is now believed that amyloid-beta oligomers (ABOs) appear in the earliest stages of AD cause memory dysfucntion through tau hyperphosphorylation, oxidative damage, and synaptic loss. Due to the inability to reverse neuronal loss, it is critical that diagnostic probes with the ability to target biomarkers that appear years before the onset of neurodegeneration. Because ABOs are considered the first toxin to appear in AD pathogenesis and thus are an excellent candidate for an early diagnostic imaging probe, we developed antibodytargeted, ABO specific PET probes using the mouse NU4 and human ACU193 antibodies. The development of such probes will allow for the early identification of those who demonstrate AD pathology, but still lack memory deficits, which would allow for the implementation of preventative measures, precise correlation of ABO buildup with the development of memory loss, tau hyperphosporylation, and the identification of therapeutics. Evidence presented here showcases the tremendous potential of NU4PET and ACU193PET as a novel diagnostic agent for AD.
Comments
Additional team members: Dr. William Klein and Dr. Erika Cline