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The Journal of Neuroscience, February 13, 2008, 28(7):1682-1687; doi:10.1523/JNEUROSCI.5242-07.2008

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Brief Communications
Axonal Transport Rates In Vivo Are Unaffected by Tau Deletion or Overexpression in Mice

Aidong Yuan,^1,2 Asok Kumar,^1,2 Corrinne Peterhoff,¹ Karen Duff,⁴ and Ralph A. Nixon^1,2,3

¹Center for Dementia Research, Nathan Kline Institute, Orangeburg, New York 10962, ²Departments of Psychiatry and ³Cell Biology, New York University School of Medicine, New York, New York 10016, and ⁴Department of Pathology and Taub Institute, Columbia University, New York, New York 10032

Correspondence should be addressed to Dr. Aidong Yuan, Center for Dementia Research, Nathan Kline Institute, New York University School of Medicine, 140 Old Orangeburg Road, Orangeburg, NY 10962. Email: yuan{at}nki.rfmh.org

Elevated tau expression has been proposed as a possible basis for impaired axonal transport in Alzheimer's disease. To address this hypothesis, we analyzed the movement of pulse radiolabeled proteins in vivo along retinal ganglion cell (RGC) axons of mice that lack tau or overexpress human tau isoforms. Here, we show that the global axonal transport rates of slow and fast transport cargoes in axons are not significantly impaired when tau expression is eliminated or increased. In addition, markers of slow transport (neurofilament light subunit) and fast transport (snap25) do not accumulate in retinas and are distributed normally along optic axons in mice that lack or overexpress tau. Finally, ultrastructural analyses revealed no abnormal accumulations of vesicular organelles or neurofilaments in RGC perikarya or axons in mice overexpressing or lacking tau. These results suggest that tau is not essential for axonal transport and that transport rates in vivo are not significantly affected by substantial fluctuations in tau expression.

Key words: tau; Alzheimer's disease; neurofilament; snap25; slow axonal transport; fast axonal transport

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Received March 7, 2007; revised Dec. 31, 2007; accepted Jan. 6, 2008.

Correspondence should be addressed to Dr. Aidong Yuan, Center for Dementia Research, Nathan Kline Institute, New York University School of Medicine, 140 Old Orangeburg Road, Orangeburg, NY 10962. Email: yuan{at}nki.rfmh.org

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