08.03.2014 Views

TRADITIONAL POSTER - ismrm

TRADITIONAL POSTER - ismrm

TRADITIONAL POSTER - ismrm

SHOW MORE
SHOW LESS

Create successful ePaper yourself

Turn your PDF publications into a flip-book with our unique Google optimized e-Paper software.

Poster Sessions<br />

2362. MR Biomarkers of Neurodegeneration in a Transgenic Mouse Model of Alzheimer's Disease<br />

Ryan Chamberlain 1 , Malgorzata Marjanska 1 , Gregory Preboske 2 , Linda Kotilinek 3 , Thomas M.<br />

Wengenack 4 , Joseph F. Poduslo 4 , Karen H. Ashe 3 , Michael Garwood 1 , Clifford R. Jack 2<br />

1 Center for Magnetic Resonance Research, University of Minnesota, Minneapolis, MN, United States; 2 Department of Radiology,<br />

Mayo Clinic, Rochester, MN, United States; 3 Department of Neurology, University of Minnesota, Minneapolis, MN, United States;<br />

4 Departments of Neurology, Neuroscience, and Biochemistry, Mayo Clinic, Rochester, MN, United States<br />

The histological abnormalities that characterize Alzheimer’s disease are commonly divided into three major classes: amyloid plaques, neurofibrillary tangles<br />

and neurodegeneration. Much work has been done to image amyloid plaques using the APP/PS1 mouse model. However, the APP/PS1 model was<br />

developed to study amyloid plaques, and neurodegenerative changes are minimal in this model. The Tg4510 mouse model recapitulates neurodegeneration<br />

mediated through over expression of mutant human tau. In this work we compare the ability of various MR techniques (volume, T1ρ, T2ρ, ADC, FA) to<br />

detect neurodegeneration in the Tg4510 mouse model compared to wild-type mice.<br />

2363. Regional Metabolic Alteration of Alzheimer¡¯s Disease in the Mouse Brain Expressed as Mutant<br />

Human APP-PS1 Using 1H HR-MAS<br />

Dong-Cheol Woo 1 , Sung-Ho Lee 2 , Do-Wan Lee 1 , Sang-Young Kim 1 , Goo-Young Kim 1 , Hyang-Shuk Rhim 1 ,<br />

Chi-Bong Choi 3 , Hwi-Yool Kim 2 , Chang-Wook Lee 1 , Bo-Young Choe 1<br />

1 The Catholic University of Korea, Seoul, Korea, Republic of; 2 Konkuk university of Korea; 3 Kyung-Hee University of Korea, Seoul,<br />

Korea, Republic of<br />

This study was to investigate the regional neurochemical profile of APP-PS1 in the mouse brain of early-stage Alzheimer¡¯s disease (AD) using 1H HR-<br />

MAS. Compared to the wild-type mice, the memory index (MI, behavioral test result) of the APP-PS1 mice at 18 weeks was not significantly different;<br />

however, the MI of the APP-PS1 mice at 35 weeks was significantly lower. The results of 1H HR-MAS showed that the [NAA+ Acet] level of the APP-PS1<br />

mice decreased in the hippocampus and temporal cortex, mIns and sIns level was increased in the entire brain which are frontal, occipital, parietal cortex,<br />

hippocampus and thalamus.<br />

2364. Magnetic Resonance Microscopy and Micro Computed Tomography of Brain Phenotypes of Two<br />

FGFR2 Mouse Models for Apert Syndrome.<br />

Thomas Neuberger 1 , Kristina Aldridge 2 , Cheryl A. Hill 2 , Jordan A. Austin 2 , Timothy M. Ryan 3 , Christopher<br />

Percival 3 , Neus Martinez-Abadias 3 , Yingli Wang 4 , Ethylin Wang Jabs 4 , Andrew G. Webb 5,6 , Joan T.<br />

Richtsmeier 3<br />

1 The Huck Institutes of the Life Sciences, Pennsylvania State University, University Park, PA, United States; 2 University of Missouri-<br />

School of Medicine; 3 Department of Anthropology, Pennsylvania State University, University Park, PA, United States; 4 Department<br />

of Genetics and Genomic Sciences, Mount Sinai School of Medicine; 5 Department of Bioengineering, Pennsylvania State University,<br />

University Park, PA, United States; 6 Department of Radiology, Leiden University Medical Centre, Leiden, Netherlands<br />

Apert syndrome (AS) is one of at least nine disorders considered members of the FGFR-1,-2, and -3-related craniosynostosis syndromes. Nearly 100% of<br />

individuals diagnosed with AS have one of two neighboring mutations on Fgfr2. The cranial phenotype associated with these two mutations includes coronal<br />

suture synostosis. Brain dysmorphology associated with AS is thought to be secondary to cranial vault or base alterations, but the variation in brain<br />

phenotypes within Apert syndrome is unexplained. Here we present novel MRM and µ-CT 3D data on brain phenotypes of mice each carrying one of the<br />

two Fgfr2 mutations associated with AS. Our data suggest that the brain is primarily affected, rather than secondarily responding to skull dysmorphogenesis.<br />

2365. A Multimodal Imaging Approach for Phenotyping of Dynein Heavy Chain Mutant Mice Cra1 Using<br />

MRI and PET/CT<br />

Detlef Stiller 1 , Thomas Kaulisch 1 , Selina Bucher 1 , Julia Tillmanns 1 , David Kind 1 , Heiko G. Niessen 1 ,<br />

Krisztina Rona-Vörös 2 , Kerstin E. Braunstein 2 , Hans-Peter Müller 2 , Luc Dupuis 3 , Albert C. Ludolph 2<br />

1 In-Vivo Imaging, Dept. of Drug Discovery Support, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach, BW, Germany;<br />

2 Dept. of Neurology, University of Ulm, Ulm, BW, Germany; 3 ISERM U692, Strasbourg, France<br />

A mouse with a point mutation in the gene encoding the motorprotein dynein is characterized by abnormal reflexes and by progressive motor and behavioral<br />

abnormalities without motor neuron degeneration. Even though previous studies showed age-dependent striatal astrocytosis and dysfunction, no in-vivo<br />

characterization of the brain has been performed yet. To investigate structural and functional alterations in the mouse brain, longitudinal MRI and [18F]-<br />

Fallypride PET were performed. In mutant mice the striatum size was significantly decreased, that of the ventricles significantly increased. PET imaging<br />

revealed a significantly reduced striatal uptake of Fallypride, supporting the theory of cell loss in the structure.<br />

2366. Gliogenesis in Live Animals Using Targeted MRI: Detecting Neural Progenitor Cells in Vivo<br />

Philip K. Liu 1 , Christina H. Liu 1<br />

1 Radiology, Mass General Hospital/Harvard Medical School, Charlestown, MA, United States<br />

Recruitment of specific cells is associated with tissue repair. Cell typing especially at the level of the DNA or RNA, has long depended on tissue biopsy of<br />

affected organs or postmortem investigation. The ability to evaluate therapies that might overcome such perturbations by using genes or cells (gene or stem<br />

cell therapies) in a host has been significantly limited. We have developed probes for specific cell type detection using mRNA targeting antisense DNA and<br />

contrast-enhanced MRI in live animals. Examples of detecting neural progenitor cells during brain repair after cerebral ischemia using targeted MRI in vivo<br />

will be presented.

Hooray! Your file is uploaded and ready to be published.

Saved successfully!

Ooh no, something went wrong!