Rachelle Crescenzi1, 2, Daniel Adler3, Paul A. Yushkevich3, Virginia M.-Y. Lee4, John A. Detre5, Arijitt Borthakur2
1Department of Biochemistry and Molecular Biophysics, University of Pennsylvania, Philadelphia, PA, United States; 2CMROI Department of Radiology, University of Pennsylvania, Philadelphia, PA, United States; 3PICSL Department of Radiology, University of Pennsylvania; 4CNDR Department of Pathology & Lab Medicine, University of Pennsylvania; 5CfN Department of Neurology, University of Pennsylvania
Alzheimers disease has two characteristic pathologies, amyloid-beta plaques and hyperphosphorylated tau protein that forms neurofibrillary tangles. We seek to study whether the PS19 mouse model of tau pathology follows the same trend in diffusion measures as Alzheimers disease patients and the amyloid-beta mouse model. Mean diffusivity (MD) and fractional anisotropy is measured in excised brains of PS19 mice and age-matched controls. In the young cohort of mice, significant differences in diffusion measures were seen in the hippocampus and cortex. While MD is reduced in younger PS19 mice, MD increases in older PS19 mice and decreases in the WT cohort.