Gilbert Hangel¹, Philipp Lazen², Sukrit Sharma², Barbara Hritoska³, Cornelius Cadrien¹, Julia Furtner⁴, Ivo Rausch⁵, Tatjana Traub-Weidinger⁶, Eva Niess², Lukas Hingerl², Stephan Gruber², Bernhard Strasser², Barbara Kiesel⁷, Matthias Preusser⁸, Thomas Roetzer-Pejrimovsky⁹, Adelheid Woehrer⁹, Wolfgang Bogner², Georg Widhalm⁷, Karl Rössler⁷, and Siegfried Trattnig^2,10,11
1Department of Neurosurgery & High Field MR Centre, Medical University of Vienna, Wien, Austria, ²High Field MR Centre, Department of Biomedical Imaging and Image-guided Therapy, Medical University of Vienna, Vienna, Austria, ³FH Campus Wien University of Applied Sciences, Vienna, Austria, ⁴Division of Neuroradiology and Musculoskeletal Radiology, Department of Biomedical Imaging and Image-guided Therapy, Medical University of Vienna, Vienna, Austria, ⁵Center for Medical Physics and Biomedical Engineering,, Medical University of Vienna, Vienna, Austria, ⁶Division of Nuclear Medicine, Department of Biomedical Imaging and Image-guided Therapy, Medical University of Vienna, Vienna, Austria, ⁷Department of Neurosurgery, Medical University of Vienna, Vienna, Austria, ⁸Division of Oncology, Department of Internal Medicine I, Medical University of Vienna, Vienna, Austria, ⁹Division of Neuropathology and Neurochemistry, Department of Neurology, Medical University of Vienna, Vienna, Austria, ¹⁰Institute for Clinical Molecular MRI, Karl Landsteiner Society, St. Pölten, Austria, ¹¹Christian Doppler Laboratory for Clinical Molecular MR Imaging, Vienna, Austria

We compared metabolic ratio maps of tCho, Gln, and Gly to tNAA and tCr derived from high-resolution 7T MRSI to clinical amino acid PET in 24 glioma patients. We achieved the highest DICE coefficient of 0.66±0.25 for Gln/tNAA, and further defined hot spot volumes and center of intensity distances between PET and MRSI. Overall, we showed that the information content of 7T MRSI results in a better correspondence to PET as clinical gold standard than previous MRSI studies.

Hélène Roumes¹, Charlotte Jollé², Jordy Blanc¹, Imad Benkhaled^1,3, Philippe Massot¹, Marc Biran¹, Carolina Piletti Chatain⁴, Gérard Raffard¹, Véronique Bouchaud¹, Nicole Deglon⁵, Eduardo R Zimmer⁶, Luc Pellerin⁷, and Anne-Karine Bouzier-Sore^1
1CRMSB, Bordeaux, France, ²Department of Physiology, Lausanne, Switzerland, ³I3M, Poitiers, France, ⁴Department of Biochemistry, Porto Alegre, Brazil, ⁵Laboratory of Cellular and Molecular Neurotherapies, Lausanne, Switzerland, ⁶Department of Pharmacology,, Porto Alegre, Brazil, ⁷IRTOMIT, Poitiers, France

For decades, it was claimed that glucose was the sole and sufficient energy substrate to sustain neuronal activity and brain function. Our results challenge this view by demonstrating that despite glucose availability, lactate shuttling from astrocytes to neurons via monocarboxylate transporters is necessary to give rise to the BOLD signal in the rat cerebral cortex following whisker stimulation. Moreover, lactate shuttling turned out to be also essential for sustaining behavioral performance associated with activation of the rat barrel cortex. These findings call for a reappraisal of neuroenergetics and the role of astrocytes in determining brain activation and function.

Chloé Najac¹, Vincent O. Boer², Nadine A.M.E. van der Beek³, Ans T. van der Ploeg⁴, Itamar Ronen¹, Johanna M.P. van den Hout⁴, and Hermien E. Kan^1
1C.J. Gorter Center for High Field MRI, Department of Radiology, Leiden, Netherlands, ²Danish Research Centre for Magnetic Resonance, Centre for Functional and Diagnostic Imaging and Research, Copenhagen University Hospital Amager and Hvidovre, Copenhagen, Denmark, ³Center for Lysosomal and Metabolic diseases, Department of Neurology, Erasmus MC University Medical Center, Rotterdam, Netherlands, ⁴Center for Lysosomal and Metabolic diseases, Department of Pediatrics, Erasmus MC University Medical Center, Rotterdam, Netherlands

Pompe disease is caused by an abnormal accumulation of  glycogen in the lysosomes of multiple tissues including the brain due to a deficit in acid α-glucosidase (GAA). The development of enzyme replacement therapy with recombinant human GAA (rhGAA) has dramatically improved patients’ survival, however, rhGAA does not reach the brain which remains untreated. Consequently, classic-infantile Pompe patients may develop progressive white matter lesions and cognitive problems. Here, we used single-voxel ¹H MRS and spectroscopic imaging and found an accumulation of  glycogen and significant decrease in total-N-acetyl-aspartate in the brain of classic-infantile patients (n=3) when compared to age-matched healthy controls (n=3).

Simone Poli^1,2, Ahmed Fahiem Emara³, Edona Ballabani³, Angeline Buser³, Luc Tappy³, Lia Bally³, and Roland Kreis^1,2
1Magnetic Resonance Methodology, Institute of Diagnostic and Interventional Neuroradiology, University of Bern, Bern, Switzerland, ²Translational Imaging Center, sitem-insel, Bern, Switzerland, ³Department of Diabetes, Endocrinology, Nutritional Medicine and Metabolism UDEM, Insel Hospital, University Hospital Bern, Bern, Switzerland

An interleaved ²H-MRSI / ¹³C-MRS protocol to obtain a complete picture of glucose turnover in the human liver at 7T is presented. A dedicated triple-tuned surface coil was used and the setup was optimized for temporal and spatial resolution, SNR (under the restraints of SAR) and robustness to assess hepatic glucose uptake and glycogen production. Data quality and initial kinetic data after oral deuterated glucose load is reported. Further optimization is intended to establish absolute concentrations and to generate kinetic models of metabolic fluxes.

Sophia Swago¹, Abigail Cember², Puneet Bagga³, Neil Wilson², Mark A. Elliott², Ravi Prakash Reddy Nanga², Ravinder Reddy², and Walter Witschey^2
1Department of Bioengineering, University of Pennsylvania, Philadelphia, PA, United States, ²Department of Radiology, University of Pennsylvania, Philadelphia, PA, United States, ³St. Jude Children's Research Hospital, Memphis, TN, United States

In the ¹H magnetic resonance (MR) spectrum of human muscle, non-exchangeable proton resonances have been observed at 8.0, 8.2 and 8.5 ppm. While relaxation rate enhancement of these resonances was previously observed, their cross-relaxation rates with bulk water have not yet been determined. Knowledge of cross-relaxation rates could improve the design of MR techniques or serve as a potential biomarker. We quantify the cross-relaxation rate of these resonances with bulk water using selective and non-selective inversion-recovery downfield MRS at 7T. We observed the cross-relaxation rates of the 8.2 and 8.5 ppm resonances were significantly faster than the 8.0 ppm resonance.

Francesca Branzoli^1,2, Dinesh K Deelchand³, Roberto Liserre⁴, Pietro Luigi Poliani⁵, Lucia Nichelli⁶, Marc Sanson^2,7, Stéphane Lehéricy^1,2,6, and Małgorzata Marjańska^3
1Center for Neuroimaging Research - CENIR, Paris Brain Institute - ICM, Paris, France, ²UMR S 1127, Inserm U 1127, CNRS UMR 7225, Sorbonne University, Paris, France, ³Center for Magnetic Resonance Research, Department of Radiology, University of Minnesota, Minneapolis, MN, United States, ⁴Department of Radiology, Neuroradiology Unit, ASST Spedali Civili University Hospital, Brescia, Italy, ⁵Pathology Unit, Department of Molecular and Translational Medicine, Brescia University, Brescia, Italy, ⁶Department of Neuroradiology, Pitié Salpêtrière hospital, Paris, France, ⁷Department of Neurology 2, Pitié Salpêtrière hospital, Paris, France

We reported the ability of PRESS to detect cystathionine in vivo in patients with glioma and the effect of the omission of cystathionine on the quantification of the full neurochemical profile. We showed that the omission of cystathionine from analysis leads to severe biases on the quantification of other metabolites involved in cancer metabolism, e.g., aspartate, betaine, citrate, GABA and serine. Because cystathionine was shown to accumulate preferentially in gliomas with 1p/19q codeletion, omission of this metabolite may lead to the wrong evaluation of other metabolic changes in these tumors.