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Summary: Disruption of fast axonal transport is a pathogenic
mechanism for intraneuronal amyloid beta
G. Piginoa,b
, G. Morfinia,b
, Y. Atagia,b
, A. Deshpandec
, C. Yua
, L. Jungbauera
, M. LaDua
, J. Busciglioc
, and S. Bradya,b,1
aDepartment of Anatomy and Cell Biology, University of Illinois, Chicago, IL 60612; bMarine Biological Laboratory, Woods Hole, MA 02543;
and cDepartments of Neurobiology and Behavior, University of California, Irvine, CA 92697
Communicated by Rodolfo R. Llinas, New York University Medical Center, New York, NY, February 5, 2009 (received for review November 12, 2008)
The pathological mechanism by which A causes neuronal dysfunc-
tion and death remains largely unknown. Deficiencies in fast axonal
transport (FAT) were suggested to play a crucial role in neuronal
dysfunction and loss for a diverse set of dying back neuropathologies
including Alzheimer's disease (AD), but the molecular basis for patho-
logical changes in FAT were undetermined. Recent findings indicate
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