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

Journal article

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 ...

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Authors: Shipton, O; Leitz, JR; Dworzak, J; Acton, C; Tunbridge, E

• Publication status: Published
• Journal: Journal of neuroscience : the official journal of the Society for Neuroscience
• Volume: 31
• Issue: 5
• Pages: 1688-1692
• Publication date: 2011-02-01
• DOI: 10.1523/jneurosci.2610-10.2011
• EISSN: 1529-2401
• ISSN: 0270-6474
• Language: English
• Keywords: Electrophysiology; Long-Term Potentiation; Neuronal Plasticity; Polymerase Chain Reaction; Phosphorylation; Organ Culture Techniques; Hippocampus; Animals; Mice, Knockout; Glycogen Synthase Kinase 3; Mice, Inbred C57BL; Blotting, Western; tau Proteins; Amyloid beta-Peptides; Mice; Neurons; Peptide Fragments