Title: Poster session: No behavioral deficits but evidence for altered late-phase long-term potentiation of synaptic transmission in Tau knockout mice
Authors: Van der Jeugd, Anneke
Ahmed, Tariq
Brouillette, J.
Blum, D.
Buée, L.
Balschun, Detlef
D'Hooge, Rudi #
Issue Date: Jul-2010
Host Document: FENS abstract vol:5
Conference: FENS Forum of European Neuroscience edition:7 location:Amsterdam date:3-7 July 2010
Article number: 204.1
Abstract: Tau protein has been identified as the main component of neurofibrillary tangles in tauopathies, including Alzheimer's disease (AD). In tauopathies, Tau forms aggregates and takes the form of neurofibrillary tangles (NFTs) composed of insoluble, hyper phosphorylated Tau. NFTs are distributed primarily to the entorhinal region, hippocampus and cortex. The progressive accumulation of NFTs may destabilize the microtubule system and impair axonal transport, putatively affecting both hippocampal synaptic plasticity and neurocognitive functions that depend on it.
To further investigate the consequences of pathologically modified Tau and Tau aggregates in neurodegeneration, we created Tau deficient mice. These Tau knockouts do not express the Tau protein, appear physically normal and are able to reproduce. Tau knockout mice were not distinguishable from wild type controls on motor tests (grip strength, rotarod), general exploration tests (cage activity, open field, social exploration), and in the Morris water maze, a measure of cognitive function. However, Tau knockout mice displayed differences in late-phase long-term potentiation as compared to controls. The lack of an obvious phenotype in Tau knockout mice could indicate functional redundancy between Tau and other microtubule-associated proteins
Publication status: published
KU Leuven publication type: IMa
Appears in Collections:Laboratory for Biological Psychology
# (joint) last author

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