Abeta oligomer-mediated long-term potentiation impairment involves protein phosphatase 1-dependent mechanisms.

@article{Knobloch2007AbetaOL,
  title={Abeta oligomer-mediated long-term potentiation impairment involves protein phosphatase 1-dependent mechanisms.},
  author={Marlen Knobloch and M{\'e}lissa Farinelli and Uwe Konietzko and Roger M. Nitsch and Isabelle M Mansuy},
  journal={The Journal of neuroscience : the official journal of the Society for Neuroscience},
  year={2007},
  volume={27 29},
  pages={7648-53}
}
Amyloid beta (Abeta) oligomers are derived from proteolytic cleavage of amyloid precursor protein (APP) and can impair memory and hippocampal long-term potentiation (LTP) in vivo and in vitro. They are recognized as the primary neurotoxic agents in Alzheimer's disease. The mechanisms underlying such toxicity on synaptic functions are complex and not fully understood. Here, we provide the first evidence that these mechanisms involve protein phosphatase 1 (PP1). Using a novel transgenic mouse… CONTINUE READING

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