Abstract #3739

Investigation into the origin of the APT MRI signal in ischemic stroke

Kevin J Ray¹, James R Larkin¹, Brad A Sutherland^2,3, George Harston², Andrew Baldwin⁴, Alastair M Buchan², Peter Jezzard⁵, James Kennedy², Michael A Chappell⁶, and Nicola R Sibson¹

¹Oxford Institute for Radiation Oncology, Department of Oncology, University of Oxford, Oxford, United Kingdom, ²Acute Stroke Programme and Acute Vascular Imaging Centre, Radcliffe Department of Medicine, University of Oxford, Oxford, United Kingdom, ³School of Medicine, Faculty of Health, University of Tasmania, Hobart, Australia, ⁴Physical and Theoretical Chemistry Laboratory, Department of Chemistry, University of Oxford, Oxford, United Kingdom, ⁵Oxford Centre for Functional MRI of the Brain, Nuffield Department of Clinical Neurosciences, University of Oxford, Oxford, United Kingdom, ⁶Institute of Biomedical Engineering, Department of Engineering Science, University of Oxford, Oxford, United Kingdom

Studies employing CEST MRI to study ischemic stroke focus on the sensitivity of amide proton transfer (APT) MRI signals to tissue pH, assuming identical intracellular protein concentration as healthy tissue. This study shows that whilst cytoplasmic protein concentration remains stable in penumbral stroke regions, it decreases in the infarct core. By analysing APT MRI data with APTR*, which is specifically sensitive to amide proton exchange effects, we demonstrate that the APT signal change in infarct core is dominated by decreased protein concentration, whilst penumbral APT changes can be attributed to decreased tissue pH.

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