Neuroscience 2004 Abstract
| Presentation Number: | 478.7 |
|---|---|
| Abstract Title: | A potential MRI contrast agent targeting Alzheimer's amyloid. |
| Authors: |
Huang, X.*1
; Dedeoglu, A.2
; Rosen, B. R.1
; Jenkins, B. G.1
1Psychiatry/Genet. & Aging Res. Unit, MGH/ Harvard Med. Sch., Charlestown, MA 2Radiology/Martinos Biomed. Imaging Ctr., MGH/ Harvard Med. Sch., Charlestown, MA |
| Primary Theme and Topics |
Techniques in Neuroscience - Staining, tracing and imaging techniques |
| Secondary Theme and Topics | Neurological and Psychiatric Conditions<br />- Neurodegenerative Disorders<br />-- Alzheimer's Disease: Neuropharmacology and neurotransmitters |
| Session: |
478. Imaging Techniques: MRI, fMRI, and PET Slide |
| Presentation Time: | Monday, October 25, 2004 2:30 PM-2:45 PM |
| Location: | San Diego Convention Center - Room 2 |
| Keywords: | Abeta, Gadolinium, DTPA, Molecular Imaging |
Background and Objective: Currently, there is no in vivo detection method for Alzheimer’s Abeta amyloidosis is available clinically. This study is to develop amyloid-specific in vivo imaging compounds for detecting and monitoring Alzheimer's disease Abeta amyloidogenesis.
Methods: A novel amyloid-targeting Gadolinium (Gd) metal complex- Gd-XH1 has been designed, synthesized, and chemically characterized. MRI measurements (3T magnetic field strength) were made for solution mixes of Gd-XH1 complex and Abeta40/42 peptides, human serum albumin (HSA), or AD mouse and human brain tissue extracts filled in 4.5-mL hollow polypropylene plastic spheres (phantoms). The effects of Gd-XH1 on longitudinal (T1) magnetic relaxation rates were reported. Gd-DTPA was used as control MRI contrast imaging agent. We have also performed some preliminary studies on rodent models using Gd-XH1.
Results: MRI phantom experiment shows that T1 decreases as the Abeta peptide concentration increases. There were little T1 signal changes when Gd-DTPA interacts with either HSA or Abeta peptides. In addition, T1 signals are enhanced in AD transgenic mouse and human brain tissue extracts when mixed with Gd-XH1. Furthermore, MRI signals increase in a rat brain after i.p. injection of Gd-XH1. The increase of T1-weighted signal intensity (4.7 T magnetic field strength) appears to be widespread after injection indicating significant permeability to the compound in both brain and skeletal muscle. The MRI study of Gd-XH1 on the transgenic mice is currently underway.
Conclusions: Gd-XH1 complex may interact specifically with Abeta peptides in vitro and ex vivo. Thus, Gd-XH1 could be a potential MRI contrast agents targeting Alzheimer’s Abeta amyloid in vivo.
Methods: A novel amyloid-targeting Gadolinium (Gd) metal complex- Gd-XH1 has been designed, synthesized, and chemically characterized. MRI measurements (3T magnetic field strength) were made for solution mixes of Gd-XH1 complex and Abeta40/42 peptides, human serum albumin (HSA), or AD mouse and human brain tissue extracts filled in 4.5-mL hollow polypropylene plastic spheres (phantoms). The effects of Gd-XH1 on longitudinal (T1) magnetic relaxation rates were reported. Gd-DTPA was used as control MRI contrast imaging agent. We have also performed some preliminary studies on rodent models using Gd-XH1.
Results: MRI phantom experiment shows that T1 decreases as the Abeta peptide concentration increases. There were little T1 signal changes when Gd-DTPA interacts with either HSA or Abeta peptides. In addition, T1 signals are enhanced in AD transgenic mouse and human brain tissue extracts when mixed with Gd-XH1. Furthermore, MRI signals increase in a rat brain after i.p. injection of Gd-XH1. The increase of T1-weighted signal intensity (4.7 T magnetic field strength) appears to be widespread after injection indicating significant permeability to the compound in both brain and skeletal muscle. The MRI study of Gd-XH1 on the transgenic mice is currently underway.
Conclusions: Gd-XH1 complex may interact specifically with Abeta peptides in vitro and ex vivo. Thus, Gd-XH1 could be a potential MRI contrast agents targeting Alzheimer’s Abeta amyloid in vivo.
Supported by NIMH/NIH and AFAR
Sample Citation:
[Authors]. [Abstract Title]. Program No. XXX.XX. 2004 Neuroscience Meeting Planner. San Diego, CA: Society for Neuroscience, 2004. Online.
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