Autophagy-related protein 7 deficiency in amyloid β (Aβ) precursor protein transgenic mice decreases Aβ in the multivesicular bodies and induces Aβ accumulation in the Golgi.

@article{Nilsson2015AutophagyrelatedP7,
  title={Autophagy-related protein 7 deficiency in amyloid β (Aβ) precursor protein transgenic mice decreases Aβ in the multivesicular bodies and induces Aβ accumulation in the Golgi.},
  author={Per Nilsson and Misaki Sekiguchi and Takumi Akagi and Shinichi Izumi and Toshihisa Komori and Kelvin Kai-Wan Hui and Karin Margareta S{\"o}rgjerd and Motomasa Tanaka and Takashi Saito and Nobuhisa Iwata and Takaomi C Saido},
  journal={The American journal of pathology},
  year={2015},
  volume={185 2},
  pages={305-13}
}
Alzheimer disease (AD) is biochemically characterized by increased levels of amyloid β (Aβ) peptide, which aggregates into extracellular Aβ plaques in AD brains. Before plaque formation, Aβ accumulates intracellularly in both AD brains and in the brains of AD model mice, which may contribute to disease progression. Autophagy, which is impaired in AD, clears cellular protein aggregates and participates in Aβ metabolism. In addition to a degradative role of autophagy in Aβ metabolism we recently… CONTINUE READING
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