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The Journal of Neuroscience, October 14, 2009, 29(41):12776-12786; doi:10.1523/JNEUROSCI.3463-09.2009

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Symposia and Mini-Symposia
Axonal Transport Defects in Neurodegenerative Diseases

Gerardo A. Morfini,¹ Matthew Burns,¹ Lester I. Binder,² Nicholas M. Kanaan,² Nichole LaPointe,² Daryl A. Bosco,³ Robert H. Brown Jr,³ Hannah Brown,⁴ Ashutosh Tiwari,⁵ Lawrence Hayward,³ Julia Edgar,⁶ Klaus-Armin Nave,⁷ James Garberrn,⁸ Yuka Atagi,¹ Yuyu Song,¹ Gustavo Pigino,¹ and Scott T. Brady¹

¹Department of Anatomy and Cell Biology, University of Illinois at Chicago, Chicago, Illinois 60612, ²Department of Cell and Molecular Biology, Feinberg School of Medicine, Northwestern University, Chicago, Illinois 60611, ³Department of Neurology, University of Massachusetts Medical Center, Worcester, Massachusetts 01655, ⁴Department of Psychiatry, Massachusetts General Hospital, Boston, Massachusetts 02114, ⁵Department of Chemistry, Michigan Technological University, Houghton, Michigan 49931, ⁶Applied Neurobiology Group, Division of Cell Sciences, Institute of Comparative Medicine, University of Glasgow, G61 1QH Glasgow, Scotland, ⁷Department of Neurogenetics, Max Planck Institute of Experimental Medicine, D-37075 Göttingen, Germany, and ⁸Department of Neurology and Center for Molecular Medicine and Genetics, Wayne State University School of Medicine, Detroit, Michigan 48201

Correspondence should be addressed to Dr. Gerardo A. Morfini, Department of Anatomy and Cell Biology, University of Illinois at Chicago, MC512, 909 South Wolcott Street, COMRB Room 6051, Chicago, IL 60612. Email: gmorfini{at}uic.edu

Adult-onset neurodegenerative diseases (AONDs) comprise a heterogeneous group of neurological disorders characterized by a progressive, age-dependent decline in neuronal function and loss of selected neuronal populations. Alterations in synaptic function and axonal connectivity represent early and critical pathogenic events in AONDs, but molecular mechanisms underlying these defects remain elusive. The large size and complex subcellular architecture of neurons render them uniquely vulnerable to alterations in axonal transport (AT). Accordingly, deficits in AT have been documented in most AONDs, suggesting a common defect acquired through different pathogenic pathways. These observations suggest that many AONDs can be categorized as dysferopathies, diseases in which alterations in AT represent a critical component in pathogenesis. Topics here address various molecular mechanisms underlying alterations in AT in several AONDs. Illumination of such mechanisms provides a framework for the development of novel therapeutic strategies aimed to prevent axonal and synaptic dysfunction in several major AONDs.

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Received July 17, 2009; accepted Aug. 4, 2009.

Correspondence should be addressed to Dr. Gerardo A. Morfini, Department of Anatomy and Cell Biology, University of Illinois at Chicago, MC512, 909 South Wolcott Street, COMRB Room 6051, Chicago, IL 60612. Email: gmorfini{at}uic.edu

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Neurofilaments in axonal neuropathy

Heikki Savolainen

J. Neurosci. Online, 16 Oct 2009 [Full text]

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