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Abstract #2898

Can CEST be used as biomarker in Huntington’s disease?

Marilena Rega1,2, James Fairney1, Francisco Torrealdea1,3, Blair Leavitt4, Rachel Schahill1, Raymund Roos5, Bernhard Landwehrmeyer6, Beth Borowsky7, Sarah Tabrizi1, and Xavier Golay1

1Institute of Neurology, University College London, London, United Kingdom, 2Medical Physics, University College London Hospital, London, United Kingdom, 3Center of Medical Imaging, University College London, London, United Kingdom, 4Department of Medical Genetics, University of British Columbia, Vancouver, BC, Canada, 5Department of Neurology, University Medical Center, Leiden, United Kingdom, 6Department of Neurology, Ulm University, Ulm, Germany, 7HighQ foundation, CHDI, New York, NY, United States

Huntington’s is a hereditary disease caused by the HTT gene, resulting in the aggregation of mutant huntingtin in the cytoplasm. CEST, known to be affected by protein concentration and structure, was considered a potential biomarker for a clinical trial and comparison with MT, T1 and T2 relaxometry. Data were acquired in n=54 HD patients and n=46 healthy individuals. Comparison of CEST revealed significant differences (p<0.05) in the putamen and globus pallidus regions which did not correlate with any changes in relaxometry or MT, suggesting that CEST might be able to provide additional contrast to the already existing methods.

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