Neuroscience 2003 Abstract
| Presentation Number: | 203.7 |
|---|---|
| Abstract Title: | <I>in vivo</I> magnetic resonance imaging of amyloid plaques in AD model mice. |
| Authors: |
Wisniewski, T.*1,2,3
; Sigurdsson, E. M.2
; Wadghiri, Y. Z-.5
; Sadowski, M.1
; Scholtzova, H.1
; Tang, C. Y-.
; Aguilnaldo, G.
; Duff, K.2,6
; Turnbull, D. H.4,5
1Neurol., NYU, Sch. Med, New York, NY 2Psychiatry, NYU, Sch. Med, New York, NY 3Pathology, NYU, Sch. Med, New York, NY 4Radiology, NYU, Sch. Med, New York, NY 5NY, Millhauser Lab, HN 419, 10016, 6USA, Millhauser Lab, HN 419, 10016, |
| Primary Theme and Topics |
Neurological and Psychiatric Conditions - Neurodegenerative Disorders -- Alzheimer's Disease: Other |
| Secondary Theme and Topics | Techniques in Neuroscience<br />- Staining, tracing and imaging techniques |
| Session: |
203. Alzheimer's Disease: Imaging & Neuropathology Poster |
| Presentation Time: | Sunday, November 9, 2003 10:00 AM-11:00 AM |
| Location: | Morial Convention Center - Hall F-I, Board # JJ2 |
| Keywords: | AGING, TRANSGENIC, ALZHEIMER |
Amyloid deposition in Alzheimer’s disease (AD) occurs many years before cognitive impairment. Brain imaging techniques targeting plaques will have an important diagnostic value and may help in identifying individuals in preclinical stages of AD. Magnetic resonance imaging (MRI) has a much higher resolution than positron enhanced tomography (PET) imaging and, therefore, is a more sensitive method to detect amyloid plaques. In our initial proof-of-concept studies (Magnetic Resonance in Medicine, in press), we utilized Aβ1-40 peptide, labeled with gadolinium or monocrystalline iron oxide nanoparticles (MION). When either of these ligands is injected in vivo systemically with mannitol to transiently open the blood-brain-barrier, we are able to image ex vivo the majority of Aβ plaques in Tg mice. Using Gd labeled Aβ1-40 and in vivo μMRI, we can also detect a substantial percentage of amyloid lesions. There is a high correlation between the numerical density of Aβ plaques detected by μMRI and by immunohistochemistry. Clinical use of Aβ1-40 is not feasible because it may add to the plaque burden. As a safer approach, we are using gadolinium labeled K6Aβ1-30, a non-toxic Aβ derivative with low propensity to form β-sheet, while maintaining high affinity for Aβ. Our initial findings indicate that this compound has a similar effect as gadolinium labeled Aβ1-40 in allowing in vivo detection of amyloid plaques in Tg mice. We are currently exploring various ways to enhance the uptake of this compound into the brain. This approach may lead to a diagnostic MRI method to detect Aβplaques in AD patients.
Supported by NIH grants AG20245, AG17617 and AG20197
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2003 Neuroscience Meeting Planner. New Orleans, LA: Society for Neuroscience, 2003. Online.
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