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Abstract #4254

Kinesin Mutations Induce Defects in Mn2+ Transport in the Important Memory Circuit from Hippocampus to Basal Forebrain

Elaine L. Bearer1,2, Octavian Biris3, Xiaowei Zhang2, Russell E. Jacobs2

1Pathology, University of New Mexico, Albuquerque, NM, United States; 2Biology, California Institute of Technology, Pasadena, CA, United States; 3Engineering, Brown University, Providence, Rho Island, United States

Axonal defects underlie many human brain degenerative diseases. MEMRI has the potential to detect these defects early and to determine their biological basis. The kinesin family of microtubule motors drives vesicular transport in the brain. Trangenic mice lacking a subunit of kinesin 1, KLC1 KO, display decreased transport in peripheral nerves, increased Abeta plaques, and decreased transport in the optic nerve. We present MEMRI of the hippocampal circuit in 10 KLC KO and WT mice imaged by time-lapse MR at 11.7T and analyzed by SPM. Results show that transport defects occur in the CNS and can be detected by MEMRI.