The E693Delta mutation in amyloid precursor protein increases intracellular accumulation of amyloid beta oligomers and causes endoplasmic reticulum stress-induced apoptosis in cultured cells.

@article{Nishitsuji2009TheEM,
  title={The E693Delta mutation in amyloid precursor protein increases intracellular accumulation of amyloid beta oligomers and causes endoplasmic reticulum stress-induced apoptosis in cultured cells.},
  author={Kazuchika Nishitsuji and Takami Tomiyama and Kenichi Ishibashi and Kazuhiro Ito and Rie Teraoka and Mary P. Lambert and William L. Klein and Hiroshi Mori},
  journal={The American journal of pathology},
  year={2009},
  volume={174 3},
  pages={
          957-69
        }
}
The E693Delta mutation within the amyloid precursor protein (APP) has been suggested to cause dementia via the enhanced formation of synaptotoxic amyloid beta (Abeta) oligomers. However, this mutation markedly decreases Abeta secretion, implying the existence of an additional mechanism of neuronal dysfunction that is independent of extracellular Abeta. We therefore examined the effects of this mutation on both APP processing to produce Abeta as well as subcellular localization and accumulation… CONTINUE READING
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