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Axonal transport and neurodegenerative disease: vesicle-motor complex formation and their regulation

Authors Anderson E, White II J, Gunawardena S

Received 13 November 2013

Accepted for publication 14 January 2014

Published 10 March 2014 Volume 2014:4 Pages 29—47

DOI https://doi.org/10.2147/DNND.S57502

Checked for plagiarism Yes

Review by Single-blind

Peer reviewer comments 2


Eric N Anderson,* Joseph A White II,* Shermali Gunawardena

Department of Biological Sciences, The State University of New York at Buffalo, Buffalo, NY, USA

*These authors contributed equally to this work

Abstract: The process of axonal transport serves to move components over very long distances on microtubule tracks in order to maintain neuronal viability. Molecular motors – kinesin and dynein – are essential for the movement of neuronal cargoes along these tracks; defects in this pathway have been implicated in the initiation or progression of some neurodegenerative diseases, suggesting that this process may be a key contributor in neuronal dysfunction. Recent work has led to the identification of some of the motor-cargo complexes, adaptor proteins, and their regulatory elements in the context of disease proteins. In this review, we focus on the assembly of the amyloid precursor protein, huntingtin, mitochondria, and the RNA-motor complexes and discuss how these may be regulated during long-distance transport in the context of neurodegenerative disease. As knowledge of these motor-cargo complexes and their involvement in axonal transport expands, insight into how defects in this pathway contribute to the development of neurodegenerative diseases becomes evident. Therefore, a better understanding of how this pathway normally functions has important implications for early diagnosis and treatment of diseases before the onset of disease pathology or behavior.

Keywords: kinesin, dynein, amyloid precursor protein, huntingtin, microtubules

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