Advisor(s)
Kirsten Viola, Northwestern University
Location
Room Café
Start Date
26-4-2019 2:10 PM
End Date
26-4-2019 2:35 PM
Abstract
One of the largest improvements in the diagnosis of Alzheimer's disease (AD) has been the use of in vivo imaging methods on various species to detect the presence of amyloid fibrils. However later studies have shown that these fibrils are not closely linked to the development of the disease. Current research suggests that early stage biomarkers which instigate memory loss consist of Aβ oligomers (AβOs). AβOs accumulate early in AD and experimentally cause memory dysfunction and major cellular pathologies (e.g., tau abnormalities, synapse loss, neurological damage, etc.). Thus, AβOs are widely regarded as the isoform of Aβ responsible for AD pathology.
A valuable and important resource currently unavailable to clinicians and researchers is a means to image buildup of AβOs in vivo. Currently, MRI is used to quantify brain volume or measure brain metabolism. Available probes identify amyloid plaques and are not useful for imaging AβOs. With an AβO probe it would be possible to correlate AβO buildup with resulting cognitive pathology, providing a new means to investigate the AβO hypothesis and to assess the effectiveness of new drugs.
AβOs are now regarded as one of the first toxins to appear in disease progression, and they provide an excellent target for early diagnostic imaging. Our findings suggest that the AβO-targeted probes are not only useful for the early diagnosis of AD, but also for tracking the effectiveness of new drugs. Recent finding also suggest these probes are themselves therapeutic. Our long-term goal is to develop a diagnostic for early prodromal detection of AD and for evaluating the effectiveness of new drugs related to AD onset.
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Diagnostic Imaging and Therapy of Amyloid Beta Oligomers
Room Café
One of the largest improvements in the diagnosis of Alzheimer's disease (AD) has been the use of in vivo imaging methods on various species to detect the presence of amyloid fibrils. However later studies have shown that these fibrils are not closely linked to the development of the disease. Current research suggests that early stage biomarkers which instigate memory loss consist of Aβ oligomers (AβOs). AβOs accumulate early in AD and experimentally cause memory dysfunction and major cellular pathologies (e.g., tau abnormalities, synapse loss, neurological damage, etc.). Thus, AβOs are widely regarded as the isoform of Aβ responsible for AD pathology.
A valuable and important resource currently unavailable to clinicians and researchers is a means to image buildup of AβOs in vivo. Currently, MRI is used to quantify brain volume or measure brain metabolism. Available probes identify amyloid plaques and are not useful for imaging AβOs. With an AβO probe it would be possible to correlate AβO buildup with resulting cognitive pathology, providing a new means to investigate the AβO hypothesis and to assess the effectiveness of new drugs.
AβOs are now regarded as one of the first toxins to appear in disease progression, and they provide an excellent target for early diagnostic imaging. Our findings suggest that the AβO-targeted probes are not only useful for the early diagnosis of AD, but also for tracking the effectiveness of new drugs. Recent finding also suggest these probes are themselves therapeutic. Our long-term goal is to develop a diagnostic for early prodromal detection of AD and for evaluating the effectiveness of new drugs related to AD onset.