Age-dependent accumulation of soluble amyloid beta (Abeta) oligomers reverses the neuroprotective effect of soluble amyloid precursor protein-alpha (sAPP(alpha)) by modulating phosphatidylinositol 3-kinase (PI3K)/Akt-GSK-3beta pathway in Alzheimer mouse model.

@article{Jimnez2011AgedependentAO,
  title={Age-dependent accumulation of soluble amyloid beta (Abeta) oligomers reverses the neuroprotective effect of soluble amyloid precursor protein-alpha (sAPP(alpha)) by modulating phosphatidylinositol 3-kinase (PI3K)/Akt-GSK-3beta pathway in Alzheimer mouse model.},
  author={Sebasti{\'a}n Jim{\'e}nez and Manuel Torres and Marisa Vizuete and Raquel S{\'a}nchez-Varo and Elisabeth S{\'a}nchez-Mej{\'i}as and Laura Trujillo-Estrada and Irene Carmona-Cuenca and Cristina Caballero and Diego Ruano and Antonia Gutierrez and Javier Vitorica},
  journal={The Journal of biological chemistry},
  year={2011},
  volume={286 21},
  pages={18414-25}
}
Neurotrophins, activating the PI3K/Akt signaling pathway, control neuronal survival and plasticity. Alterations in NGF, BDNF, IGF-1, or insulin signaling are implicated in the pathogenesis of Alzheimer disease. We have previously characterized a bigenic PS1×APP transgenic mouse displaying early hippocampal Aβ deposition (3 to 4 months) but late (17 to 18 months) neurodegeneration of pyramidal cells, paralleled to the accumulation of soluble Aβ oligomers. We hypothesized that PI3K/Akt/GSK-3… CONTINUE READING

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