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.