Abstract #2898

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

Marilena Rega^1,2, James Fairney¹, Francisco Torrealdea^1,3, 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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