Matthew C. Murphy1, Geoffrey L. Curran2, Kevin J. Glaser1, Phillip J. Rossman1, John Huston, III1, Joseph F. Poduslo2, Clifford R. Jack1, Joel P. Felmlee1, Richard L. Ehman1
1Department of Radiology, Mayo Clinic College of Medicine, Rochester, MN, United States; 2Department of Neuroscience, Mayo Clinic College of Medicine, Rochester, MN, United States
Magnetic resonance elastography was performed in 5 wild-type (WT) mice and 5 Alzheimers disease (AD) mice. The AD model is a double mutation in amyloid precursor protein and presenilin-1 (APP-PS1), which leads to the extracellular deposition of amyloid protein and the formation of plaques with age. The AD mice were found to have a significantly lower mean stiffness compared to age-matched WT mice with a p-value of less than 0.01. The decrease in stiffness may result from mechanical changes in the extracellular matrix following amyloid deposition.