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Tau protein is required for amyloid {beta}-induced impairment of hippocampal long-term potentiation.

Publication ,  Journal Article
Shipton, OA; Leitz, JR; Dworzak, J; Acton, CEJ; Tunbridge, EM; Denk, F; Dawson, HN; Vitek, MP; Wade-Martins, R; Paulsen, O; Vargas-Caballero, M
Published in: J Neurosci
February 2, 2011

Amyloid β (Aβ) and tau protein are both implicated in memory impairment, mild cognitive impairment (MCI), and early Alzheimer's disease (AD), but whether and how they interact is unknown. Consequently, we asked whether tau protein is required for the robust phenomenon of Aβ-induced impairment of hippocampal long-term potentiation (LTP), a widely accepted cellular model of memory. We used wild-type mice and mice with a genetic knock-out of tau protein and recorded field potentials in an acute slice preparation. We demonstrate that the absence of tau protein prevents Aβ-induced impairment of LTP. Moreover, we show that Aβ increases tau phosphorylation and that a specific inhibitor of the tau kinase glycogen synthase kinase 3 blocks the increased tau phosphorylation induced by Aβ and prevents Aβ-induced impairment of LTP in wild-type mice. Together, these findings show that tau protein is required for Aβ to impair synaptic plasticity in the hippocampus and suggest that the Aβ-induced impairment of LTP is mediated by tau phosphorylation. We conclude that preventing the interaction between Aβ and tau could be a promising strategy for treating cognitive impairment in MCI and early AD.

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Published In

J Neurosci

DOI

EISSN

1529-2401

Publication Date

February 2, 2011

Volume

31

Issue

5

Start / End Page

1688 / 1692

Location

United States

Related Subject Headings

  • tau Proteins
  • Polymerase Chain Reaction
  • Phosphorylation
  • Peptide Fragments
  • Organ Culture Techniques
  • Neurons
  • Neuronal Plasticity
  • Neurology & Neurosurgery
  • Mice, Knockout
  • Mice, Inbred C57BL
 

Citation

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Shipton, O. A., Leitz, J. R., Dworzak, J., Acton, C. E. J., Tunbridge, E. M., Denk, F., … Vargas-Caballero, M. (2011). Tau protein is required for amyloid {beta}-induced impairment of hippocampal long-term potentiation. J Neurosci, 31(5), 1688–1692. https://doi.org/10.1523/JNEUROSCI.2610-10.2011
Shipton, Olivia A., Julie R. Leitz, Jenny Dworzak, Christine E. J. Acton, Elizabeth M. Tunbridge, Franziska Denk, Hana N. Dawson, et al. “Tau protein is required for amyloid {beta}-induced impairment of hippocampal long-term potentiation.J Neurosci 31, no. 5 (February 2, 2011): 1688–92. https://doi.org/10.1523/JNEUROSCI.2610-10.2011.
Shipton OA, Leitz JR, Dworzak J, Acton CEJ, Tunbridge EM, Denk F, et al. Tau protein is required for amyloid {beta}-induced impairment of hippocampal long-term potentiation. J Neurosci. 2011 Feb 2;31(5):1688–92.
Shipton, Olivia A., et al. “Tau protein is required for amyloid {beta}-induced impairment of hippocampal long-term potentiation.J Neurosci, vol. 31, no. 5, Feb. 2011, pp. 1688–92. Pubmed, doi:10.1523/JNEUROSCI.2610-10.2011.
Shipton OA, Leitz JR, Dworzak J, Acton CEJ, Tunbridge EM, Denk F, Dawson HN, Vitek MP, Wade-Martins R, Paulsen O, Vargas-Caballero M. Tau protein is required for amyloid {beta}-induced impairment of hippocampal long-term potentiation. J Neurosci. 2011 Feb 2;31(5):1688–1692.

Published In

J Neurosci

DOI

EISSN

1529-2401

Publication Date

February 2, 2011

Volume

31

Issue

5

Start / End Page

1688 / 1692

Location

United States

Related Subject Headings

  • tau Proteins
  • Polymerase Chain Reaction
  • Phosphorylation
  • Peptide Fragments
  • Organ Culture Techniques
  • Neurons
  • Neuronal Plasticity
  • Neurology & Neurosurgery
  • Mice, Knockout
  • Mice, Inbred C57BL