TRADITIONAL POSTER - ismrm

2390. In Vitro Proton MRS of Cerebral Metabolites in a Mouse Model of Alzheimer's Disease
Duncan Forster 1 , Steve Williams 2 , Mike James 3 , Jill Richardson 3
1 University of Manchester, Manchester, United Kingdom; 2 University Of Manchester; 3 GlaxoSmithKline
Poster Sessions
An in vitro proton MRS study was carried out on mice ranging from 3 to 18 months in order to investigate cerebral metabolic differences between TASTPM
Alzheimer's mice and their wild type base strain. An effect of genotype was observed for myo-inositol, with concentration being higher in TASTPM mice,
myo-inositol may therefore be an Alzheimer's marker. Lower levels of succinate were observed in TASTPM mice, being an effect of both age and genotype.
This may indicate impaired neuronal energy production or mitochondrial dysfunction. The results also call into question the use of creatine as a reference
metabolite.
2391. In Vivo 1 H MRS Measurements of Acetate in Mouse Striatum After Permanent Focal Middle Cerebral
Artery Occlusion
Hongxia Lei 1,2 , Lijing Xin 1 , Carole Berthet 3 , Lorenz Hirt 3 , Rolf Gruetter 1,4
1 LIFMET, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland; 2 Radiology, University of Lausanne, Lausanne,
Switzerland; 3 Neurology, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland; 4 Radiology, University of Geneva,
Geneva, Switzerland
1 H MRS of permanent focal middle cerebral occlusion (pMCAO) in mice could be feasible at high magnetic field. However, one of hydrolytic metabolites of
NAA, acetate (1.9ppm), was heavily overlapped by accumulated GABA (1.89ppm) after pMCAO. In this study, we demonstrated that short echo time 1 H
MRS of measuring acetate was feasible at ultra short echo time using LCModel analysis when comparing to the measurements with minimal GABA
contributions at a moderate echo time.
2392. In Vivo 1 H MR Studies of Cortical Metabolic Response During Insulin-Induced Hypoglycemia
Hongxia Lei 1,2 , Arthur W. Magill 1,2 , Vladimir Mlynarik 1 , Rolf Gruetter 1,3
1 LIFMET, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland; 2 Radiology, University of Lausanne, Lausanne,
Switzerland; 3 Radiology, University of Geneva, Geneva, Switzerland
Understanding hypoglycemia became very essential for treating diabetes in clinical. We explored 1 H MR studies, including cerebral blood flow and
neurochemical profile of cortical tissue under insulin-induced hypoglycemia in rats.
2393. Elevated Brain Lactate Measured by 1 H-MRS Is an Early Phenotype Due to Mitochondrial
Dysfunction in the Prematurely Ageing MtDNA Mutator Mouse
Jaime M. Ross 1,2 , Johana Öberg 3 , Stefan Brené 4 , Giuseppe Coppotelli 5 , Mügen Terzioglu 6 , Karin Pernold 1 ,
Rouslan Sitnikov 3 , Jan Kehr 7 , Alexandra Trifunovic 6 , Nils-Göran Larsson 6,8 , Barry J. Hoffer 2 , Lars Olson 1
1 Neuroscience, Karolinska Institutet, Stockholm, Sweden; 2 National Institute on Drug Abuse, National Institutes of Health, Baltimore,
MD, United States; 3 Clinical Science, Intervention and Technology, Karolinska Institutet, Stockholm, Sweden; 4 Neurobiology, Health
Sciences and Society, Karolinska Institutet, Stockholm, Sweden; 5 Cell and Molecular Biology, Karolinska Institutet, Stockholm,
Sweden; 6 Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden; 7 Physiology and Pharmacology, Karolinska Institutet,
Stockholm, Sweden; 8 Max Planck Institute for Biology of Ageing, Cologne, Germany
The prematurely ageing mtDNA mutator mouse was used to study mitochondrial dysfunction in the brain. 1 H-MRS detected a 2-fold increase in cortical and
striatal lactate levels as early as 6-9 weeks and continued throughout the lives of mtDNA mutator mice (average life span 45-48 weeks). Increased brain
lactate levels were confirmed postmortem by high-performance liquid chromatography (HPLC). These methods revealed that abnormally high lactate levels
in the CNS are an early phenotype of premature ageing in the mtDNA mutator mouse. Our data support the hypothesis of abnormal metabolism in ageing
due to mitochondrial dysfunction.
2394. Mouse Brain Structure and Metabolic Stability Follows Focused Beam Microwave Irradiation
Michael D. Boska 1 , Erin McIntyre 1 , Melissa Lynn Mellon 1 , Howard E. Gendelman 2
1 Radiology, University of Nebraska Medical Center, Omaha, NE, United States; 2 Pharmacology and Experimental Neurosciences,
University of Nebraska Medical Center, Omaha, NE, United States
Mouse brain structural and metabolic stability were determined by T 1 and T 2 mapping and DTI at 0.7 and 0.9 s of 4 kW FBMI and by quantitative single
voxel PRESS, respectively. Measures were taken in-vivo before and repetitively, at 1.17 hour intervals, after FBMI. Analysis continued for a total duration
of 16 hours at room temperature. The longer FBMI duration was best for maintaining metabolite levels in the mouse brain; whereas T 1 , T 2 , and DTI metrics
were best maintained by shorter duration FBMI.
2395. Coupling of Cerebral Phosphoethanolamine and Nucleotide Triphosphate Levels and Mitochondrial-
Respiration Modulation During Perinatal "secondary Energy Failure"
Ernest Brunton Cady 1 , Osuke Iwata 2 , Alan Bainbridge 1 , John Wyatt 2 , Nikki Jayne Robertson 2
1 Medical Physics & Bioengineering, UCLH NHS Foundation Trust, London, United Kingdom; 2 Institute for Women's Health,
University College London, London, United Kingdom
Phosphoethanolamine concentration ([PE]) is high in neonatal brain. [PE] reduction increases mitochondrial respiration. We aimed to elucidate PE's
metabolic role following hypoxia-ischaemia (HI). Thirty-three piglets were studied by 31P MRS (27 HI; 6 controls). For severe cerebral injury
[PE]/[exchangeable phosphate pool] fell below controls but later recovered: however, [PE]/[nucleotide triphosphate (NTP; mainly ATP)] was almost
constant suggesting strong PE to NTP coupling. In cells stressed after HI reduced [ATP] may inhibit ethanolamine phosphokinase resulting in [PE] reduction
and stimulation of ATP generation by surviving mitochondria. High neonatal [PE] may be a factor evolved to counter mammalian cerebral birth trauma.