Tau isoforms imbalance impairs the axonal transport of the amyloid ...

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Nov 11, 2016 - One sentence summary: Tau isoforms in APP axonal transport. 3. Authors. 4 .... developing brain while a balanced 3R:4R tau expression is found in the adult human. 85 ..... as indicated in the experimental timeline (Figure 1).
This Accepted Manuscript has not been copyedited and formatted. The final version may differ from this version.

Research Articles: Neurobiology of Disease

Tau isoforms imbalance impairs the axonal transport of the amyloid precursor protein in human neurons Valentina Lacovich1,2,#, Sonia L. Espindola3,#, Matías Alloatti1,#, Victorio Pozo Devoto1, Lucas Cromberg1, Mária #arná2, Giancarlo Forte2, Jean-Marc Gallo4, Luciana Bruno5, Gorazd B. Stokin2, M. Elena Avale3,* and Tomás L. Falzone1,6,* 1

Instituto de Biología Celular y Neurociencias (IBCN-CONICET-UBA), Facultad de Medicina, Universidad de Buenos Aires, Argentina. 2

Centre for Translational Medicine (CTM), International Clinical Research Center, St. Anne's University Hospital (ICRC-FNUSA), Brno, Czech Republic. 3

Instituto de Ingeniería Genética y Biología Molecular (INGEBI-CONICET), Buenos Aires, Argentina.

4

Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King's College London, United Kingdom. 5

Departamento de Física (IFIBA-CONICET), Facultad de Ciencias Exactas y Naturales (UBA), Buenos Aires, Argentina. 6

Instituto de Biología y Medicina Experimental (IBYME-CONICET), Argentina.

DOI: 10.1523/JNEUROSCI.2305-16.2016 Received: 20 July 2016 Revised: 21 September 2016 Accepted: 4 November 2016 Published: 11 November 2016

Author contributions: V.L., S.E., M.A., V.P.D., L.E.C., M.E.A., and T.L.F. performed research; S.E., M.A., M.C., L.B., M.E.A., and T.L.F. analyzed data; G.F. contributed unpublished reagents/analytic tools; J.M.G., L.B., G.S., M.E.A., and T.L.F. designed research; M.E.A. and T.L.F. wrote the paper. Conflict of Interest: The authors declare no competing financial interests. T.L.F and M.E.A acknowledge support from CONICET, University of Buenos Aires and the Argentinean Science Ministry. S.L.E., V.M.P.D., M.A., and L.E.C. receive fellowships from CONICET. This work was supported by grants from MINCyT (PICT 2013-0402, T.L.F and PICT2013-1109, M.E.A.); the Alzheimer Association (NIRG10-172840, T.L.F.), UBA (UBACyT 2011/2014, T.L.F.), the International Brain Research Organization (M.E.A), ISN-CAEN (M.E.A) and European Regional Development Fund - Project FNUSA-ICRC (No. CZ.1.05/1.1.00/02.0123, G.B.S.; LQ1605, G.B.S.). We thank Drs. Mariela Sued and Daniela Rodríguez for help with the statistical analysis of the data; Roux-Ocefa Argentina for kindly contributing with basic reagents and Fundación Rene Baron for donations. *Corresponding authors: [email protected] and [email protected] Cite as: J. Neurosci 2016; 10.1523/JNEUROSCI.2305-16.2016 Alerts: Sign up at www.jneurosci.org/cgi/alerts to receive customized email alerts when the fully formatted version of this article is published.

Accepted manuscripts are peer-reviewed but have not been through the copyediting, formatting, or proofreading process. Copyright © 2016 the authors



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Instituto de Biología Celular y Neurociencias (IBCN-CONICET-UBA), Facultad de Medicina, Universidad de Buenos Aires, Argentina. 2 Centre for Translational Medicine (CTM), International Clinical Research Center, St. Anne's University Hospital (ICRC-FNUSA), Brno, Czech Republic. 3 Instituto de Ingeniería Genética y Biología Molecular (INGEBI-CONICET), Buenos Aires, Argentina. 4 Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King’s College London, United Kingdom. 5 Departamento de Física (IFIBA-CONICET), Facultad de Ciencias Exactas y Naturales (UBA), Buenos Aires, Argentina. 6 Instituto de Biología y Medicina Experimental (IBYME-CONICET), Argentina. 

These authors contributed equally to this work.

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* Corresponding authors: [email protected] and [email protected].

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