Diagnostic Amyloid Beta Oligomer-Targeted Probes for Alzheimer’s Disease
Session Number
Project ID: MEDH 28
Advisor(s)
Kirsten Viola; Northwestern University
Discipline
Medical and Health Sciences
Start Date
22-4-2020 9:10 AM
End Date
22-4-2020 9:25 AM
Abstract
Current Alzheimer’s Disease (AD) research suggests that early stage biomarkers which instigate memory loss consist of amyloid beta proteins in the oligomer isoform (AβOs). AβOs accumulate early in AD and have been shown experimentally to cause major AD-related pathologies (e.g., tau abnormalities, synapse loss, neurological damage, etc.). However, clinicians are currently unable to image AβO buildup in vivo. MRI is used to quantify brain volume or measure brain metabolism. Available PET probes exclusively quantify amyloid plaques and are not useful for imaging AβOs. With an AβO probe, it would be possible to correlate AβO buildup with emergence of cognitive dysfunction, providing new means to investigate the AβO hypothesis and assess the experimental efficacy of investigational 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 both transgenic mice and non-transgenic dietary risk-factor-induced rabbits are effective models for investigating) accumulation of AβOs. Further, the success of AβO-targeted probes in these in vivo studies suggest they are useful not only for the early diagnosis of AD, but also for future clinical studies.
Diagnostic Amyloid Beta Oligomer-Targeted Probes for Alzheimer’s Disease
Current Alzheimer’s Disease (AD) research suggests that early stage biomarkers which instigate memory loss consist of amyloid beta proteins in the oligomer isoform (AβOs). AβOs accumulate early in AD and have been shown experimentally to cause major AD-related pathologies (e.g., tau abnormalities, synapse loss, neurological damage, etc.). However, clinicians are currently unable to image AβO buildup in vivo. MRI is used to quantify brain volume or measure brain metabolism. Available PET probes exclusively quantify amyloid plaques and are not useful for imaging AβOs. With an AβO probe, it would be possible to correlate AβO buildup with emergence of cognitive dysfunction, providing new means to investigate the AβO hypothesis and assess the experimental efficacy of investigational 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 both transgenic mice and non-transgenic dietary risk-factor-induced rabbits are effective models for investigating) accumulation of AβOs. Further, the success of AβO-targeted probes in these in vivo studies suggest they are useful not only for the early diagnosis of AD, but also for future clinical studies.