TRADITIONAL POSTER - ismrm

Poster Sessions
2356. Early Pathological Changes in the Optic Nerves of Type-I Diabetic Rats Revealed by Directional
Diffusion-Weighted MRI
Lifeng Gao 1 , Mingming Huang 1 , Hao Lei 1
1 Wuhan Institute of Physics & Mathematics, The Chinese Academy of Sciences, Wuhan, Hubei, China
Type-I diabetes was induced in rats by a single injection of streptozotocin (STZ). Directional diffusion-weighted imaging on the optic nerves were
performed at 4 weeks and 10 weeks on a 4.7 T scanner to monitor the early pathological changes induced by diabetes. Water diffusivities parallel and
perpendicular to the axonal tracts were measured by the apparent diffusion coefficients ADC // and ADC(perpendicular), respectively. Compared to the
control animals, the STZ-treated animals showed a trend of reduced ADC(perpendicular) in the optic nerves at 4 weeks, and significantly decreased
ADC(perpendicular) at 10 weeks, but insignificant changes in ADC // at these time points.
2357. Abnormalities in the Visual Pathway of Rats Subjected to Early Bilateral Enucleation Revealed by
Diffusion Tensor Imaging
Xuxia Wang 1 , Fuchun Lin 1 , Tingzhu Lin 1 , Hao Lei 1
1 Wuhan Institute of Physics & Mathematics, The Chinese Academy of Sciences, Wuhan, Hubei, China
In this study, diffusion tensor imaging and high resolution rapid-acquisition relaxation-enhancement (RARE) imaging were used to detect the morphological
and structural changes in the brain of rats subjected to early bilateral enucleation at postnatal day 4. Profound atrophy was observed in the ON and OCH of
the enucleated rats, likely a manifestation of transneuronal degeneration induced by deafferentation. The optic tract of the enucleated rats did not appear to
be atrophic, but exhibited water diffusion abnormalities resembling those found in Wallerian degeneration. The primary visual cortex of the enucleated rats
showed no changes in water diffusivity.
2358. Developmental in Vivo 1H NMR Spectroscopy at 14.1 T in Mice with Genetic Redox Dysregulation: An
Animal Model with Relevance to Schizophrenia
Joao MN Duarte 1 , Anita Kulak 2 , Kim Q. Do 2 , Rolf Gruetter 1,3
1 Center for Biomedical Imaging (CIBM), Lausanne, Vaud, Switzerland; 2 Centre for Psychiatric Neuroscience, Lausanne Univ. Hosp.,
Lausanne, Switzerland; 3 Department of Radiology, Universities of Lausane and Geneva, Lausanne, Switzerland
The present study reports alterations of the neurochemical profile in the cortex of a mouse model of redox deregulation induced by genetic reduction of
glutathione synthesis. The observed metabolic alterations suggest impaired mitochondrial metabolism and eventually altered neurotransmission, both
possibly triggering degeneration.
2359. An Automated Method to Optimize the Contrast of Small Structures
Ryan Chamberlain 1 , Thomas M. Wengenack 2 , Joseph F. Poduslo 2 , Clifford R. Jack 3 , Michael Garwood 1
1 Center for Magnetic Resonance Research, University of Minnesota, Minneapolis, MN, United States; 2 Departments of Neurology,
Neuroscience, and Biochemistry/Molecular Biology, Mayo Clinic College of Medicine, Rochester, MN, United States; 3 Department of
Radiology, Mayo Clinic College of Medicine, Rochester, MN, United States
Many MRI applications require visualizing structures on the order of a few pixels in size. In these applications the CNR ratio of the small structures is more
important than the SNR of the image. The CNR can be affected dramatically by the image resolution relative to the size of the structure, but the exact
relation of resolution and CNR depends on the specific structure and pulse sequence. This work describes an automated method to determine the acquired
image resolution to optimize the CNR of small structures. It is demonstrated as applied to imaging amyloid plaques in transgenic mouse models of
Alzheimer's disease.
2360. MR Elastography of the Brain in a Mouse Model of Alzheimer's Disease
Matthew C. Murphy 1 , Geoffrey L. Curran 2 , Kevin J. Glaser 1 , Phillip J. Rossman 1 , John Huston, III 1 , Joseph
F. Poduslo 2 , Clifford R. Jack 1 , Joel P. Felmlee 1 , Richard L. Ehman 1
1 Department of Radiology, Mayo Clinic College of Medicine, Rochester, MN, United States; 2 Department of Neuroscience, Mayo
Clinic College of Medicine, Rochester, MN, United States
Magnetic resonance elastography was performed in 5 wild-type (WT) mice and 5 Alzheimer’s disease (AD) mice. The AD model is a double mutation in
amyloid precursor protein and presenilin-1 (APP-PS1), which leads to the extracellular deposition of amyloid protein and the formation of plaques with age.
The AD mice were found to have a significantly lower mean stiffness compared to age-matched WT mice with a p-value of less than 0.01. The decrease in
stiffness may result from mechanical changes in the extracellular matrix following amyloid deposition.
2361. Cerebral Amyloid Angiopathy in Transgenic Mice Modelling Alzheimer’s Disease Studied Non-
Invasively by MRI
Nicolau Beckmann 1 , Catherine Cannet 1 , Christelle Gerard 1 , Dorothee Abramowski 2 , Matthias Staufenbiel 2
1 Global Imaging Group, Novartis Institutes for BioMedical Research, Basel, BS, Switzerland; 2 Nervous System Department, Novartis
Institutes for BioMedical Research, Basel, BS, Switzerland
MRI detected effects of cerebral amyloid angiopathy (CAA) in several lines of Alzheimer’s mice differing by amyloid-ß-40 (Aß40) contents. SPIO was
administered i.v. 24h before MRI. Signal attenuations became apparent in multiple foci throughout the brain cortex and in thalamic regions of APP23 mice
displaying high Aß40. At sites of MRI signal loss, iron was localized in microglia cells/macrophages in/or around damaged vessels. The small number of
attenuated signal foci in the brains of APP24 and APP23xPS45 mice characterized by low Aß40 was consistent with histology showing significantly less
vascular amyloid compared to APP23 animals. These results agree with Aß40 predominating in CAA-related vascular amyloid.