TRADITIONAL POSTER - ismrm

Poster Sessions
2362. MR Biomarkers of Neurodegeneration in a Transgenic Mouse Model of Alzheimer's Disease
Ryan Chamberlain 1 , Malgorzata Marjanska 1 , Gregory Preboske 2 , Linda Kotilinek 3 , Thomas M.
Wengenack 4 , Joseph F. Poduslo 4 , Karen H. Ashe 3 , Michael Garwood 1 , Clifford R. Jack 2
1 Center for Magnetic Resonance Research, University of Minnesota, Minneapolis, MN, United States; 2 Department of Radiology,
Mayo Clinic, Rochester, MN, United States; 3 Department of Neurology, University of Minnesota, Minneapolis, MN, United States;
4 Departments of Neurology, Neuroscience, and Biochemistry, Mayo Clinic, Rochester, MN, United States
The histological abnormalities that characterize Alzheimer’s disease are commonly divided into three major classes: amyloid plaques, neurofibrillary tangles
and neurodegeneration. Much work has been done to image amyloid plaques using the APP/PS1 mouse model. However, the APP/PS1 model was
developed to study amyloid plaques, and neurodegenerative changes are minimal in this model. The Tg4510 mouse model recapitulates neurodegeneration
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
detect neurodegeneration in the Tg4510 mouse model compared to wild-type mice.
2363. Regional Metabolic Alteration of Alzheimer¡¯s Disease in the Mouse Brain Expressed as Mutant
Human APP-PS1 Using 1H HR-MAS
Dong-Cheol Woo 1 , Sung-Ho Lee 2 , Do-Wan Lee 1 , Sang-Young Kim 1 , Goo-Young Kim 1 , Hyang-Shuk Rhim 1 ,
Chi-Bong Choi 3 , Hwi-Yool Kim 2 , Chang-Wook Lee 1 , Bo-Young Choe 1
1 The Catholic University of Korea, Seoul, Korea, Republic of; 2 Konkuk university of Korea; 3 Kyung-Hee University of Korea, Seoul,
Korea, Republic of
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-
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;
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
mice decreased in the hippocampus and temporal cortex, mIns and sIns level was increased in the entire brain which are frontal, occipital, parietal cortex,
hippocampus and thalamus.
2364. Magnetic Resonance Microscopy and Micro Computed Tomography of Brain Phenotypes of Two
FGFR2 Mouse Models for Apert Syndrome.
Thomas Neuberger 1 , Kristina Aldridge 2 , Cheryl A. Hill 2 , Jordan A. Austin 2 , Timothy M. Ryan 3 , Christopher
Percival 3 , Neus Martinez-Abadias 3 , Yingli Wang 4 , Ethylin Wang Jabs 4 , Andrew G. Webb 5,6 , Joan T.
Richtsmeier 3
1 The Huck Institutes of the Life Sciences, Pennsylvania State University, University Park, PA, United States; 2 University of Missouri-
School of Medicine; 3 Department of Anthropology, Pennsylvania State University, University Park, PA, United States; 4 Department
of Genetics and Genomic Sciences, Mount Sinai School of Medicine; 5 Department of Bioengineering, Pennsylvania State University,
University Park, PA, United States; 6 Department of Radiology, Leiden University Medical Centre, Leiden, Netherlands
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
individuals diagnosed with AS have one of two neighboring mutations on Fgfr2. The cranial phenotype associated with these two mutations includes coronal
suture synostosis. Brain dysmorphology associated with AS is thought to be secondary to cranial vault or base alterations, but the variation in brain
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
two Fgfr2 mutations associated with AS. Our data suggest that the brain is primarily affected, rather than secondarily responding to skull dysmorphogenesis.
2365. A Multimodal Imaging Approach for Phenotyping of Dynein Heavy Chain Mutant Mice Cra1 Using
MRI and PET/CT
Detlef Stiller 1 , Thomas Kaulisch 1 , Selina Bucher 1 , Julia Tillmanns 1 , David Kind 1 , Heiko G. Niessen 1 ,
Krisztina Rona-Vörös 2 , Kerstin E. Braunstein 2 , Hans-Peter Müller 2 , Luc Dupuis 3 , Albert C. Ludolph 2
1 In-Vivo Imaging, Dept. of Drug Discovery Support, Boehringer Ingelheim Pharma GmbH & Co. KG, Biberach, BW, Germany;
2 Dept. of Neurology, University of Ulm, Ulm, BW, Germany; 3 ISERM U692, Strasbourg, France
A mouse with a point mutation in the gene encoding the motorprotein dynein is characterized by abnormal reflexes and by progressive motor and behavioral
abnormalities without motor neuron degeneration. Even though previous studies showed age-dependent striatal astrocytosis and dysfunction, no in-vivo
characterization of the brain has been performed yet. To investigate structural and functional alterations in the mouse brain, longitudinal MRI and [18F]-
Fallypride PET were performed. In mutant mice the striatum size was significantly decreased, that of the ventricles significantly increased. PET imaging
revealed a significantly reduced striatal uptake of Fallypride, supporting the theory of cell loss in the structure.
2366. Gliogenesis in Live Animals Using Targeted MRI: Detecting Neural Progenitor Cells in Vivo
Philip K. Liu 1 , Christina H. Liu 1
1 Radiology, Mass General Hospital/Harvard Medical School, Charlestown, MA, United States
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
affected organs or postmortem investigation. The ability to evaluate therapies that might overcome such perturbations by using genes or cells (gene or stem
cell therapies) in a host has been significantly limited. We have developed probes for specific cell type detection using mRNA targeting antisense DNA and
contrast-enhanced MRI in live animals. Examples of detecting neural progenitor cells during brain repair after cerebral ischemia using targeted MRI in vivo
will be presented.