Affiliations: [a] Center for Dementia Research, Nathan Kline Institute, Orangeburg, NY, USA | [b] Department of Psychiatry, New York University School of Medicine, NY, USA | [c] Department of Cell Biology, New York University School of Medicine, NY, USA | [d] Department of Pathology and Taub Institute, Columbia University, NY, USA
Correspondence:
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Correspondence to: Aidong Yuan, M.D., Ph.D. or Ralph A. Nixon, M.D., Ph.D., Center for Dementia Research, Nathan Kline Institute, New York University School of Medicine, 140 Old Orangeburg Rd., Orangeburg, NY 10962, USA. Tel.: +1 845 398 5450; Fax: +1 845 398 5422; E-mail: [email protected] or [email protected].
Note: [1] Present address: Department of Peripheral Nervous System, National Institute of Neuroscience, National Center of Neurology and Psychiatry, Kodaira, Tokyo, Japan.
Abstract: Microtubule-based axonal transport is believed to become globally disrupted in Alzheimer's disease in part due to alterations of tau expression or phosphorylation. We previously showed that axonal transport rates along retinal ganglion axons are unaffected by deletion of normal mouse tau or by overexpression of wild-type human tau. Here, we report that htau mice expressing 3-fold higher levels of human tau in the absence of mouse tau also display normal fast and slow transport kinetics despite the presence of abnormally hyperphosphorylated tau in some neurons. In addition, markers of slow transport (neurofilament light subunit) and fast transport (snap25) exhibit normal distributions along optic axons of these mice. These studies demonstrate that human tau overexpression, even when associated with a limited degree of tau pathology, does not necessarily impair general axonal transport function in vivo.
