3D MRI and DTI of Cnp1 deficient mice: A model of axonal damage without affecting myelin
Boretius S, Goebbels S, Watanabe T, Nave K, Frahm J, Michaelis T
Max-Planck-Institut fuer biophysikalische Chemie
Genetically modified mice lacking the Cnp1 gene develop axonal swelling and neurodegeneration throughout the brain without affecting myelin, that is its ultrastructure, periodicity, and physical stability. T1- and T2-weighted 3D MRI as well as diffusion tensor imaging (DTI) revealed reduced T2 contrast as well as an increased axial and radial diffusivity of white matter. T1 contrast and FA values remained unchanged. Complementary to other animal models of human multiple sclerosis such as EAE and cuprizone-induced demyelination, Cnp1 deficient mice may allow for a better correlation of MRI contrast alteration and neurodegenerative pathology with special emphasis on axonal damage.