Suppression of Cyclin-Dependent Kinase 5 Activation by Amyloid Precursor Protein: A Novel Excitoprotective Mechanism Involving Modulation of Tau Phosphorylation

@article{Han2005SuppressionOC,
  title={Suppression of Cyclin-Dependent Kinase 5 Activation by Amyloid Precursor Protein: A Novel Excitoprotective Mechanism Involving Modulation of Tau Phosphorylation},
  author={P. Han and Fei Dou and F. Li and Xue Zhang and Yun-wu Zhang and Hui Zheng and S. Lipton and Huaxi Xu and Francesca-Fang Liao},
  journal={The Journal of Neuroscience},
  year={2005},
  volume={25},
  pages={11542 - 11552}
}
Alzheimer's disease is cytopathologically characterized by loss of synapses and neurons, neuritic amyloid plaques consisting of β-amyloid (Aβ) peptides, and neurofibrillary tangles consisting of hyperphosphorylated tau protein in susceptible brain regions. Aβ, which triggers a cascade of pathogenic events including tau phosphorylation and neuronal excitotoxicity, is proteolytically derived from β-amyloid precursor protein (APP); the pathological and physiological functions of APP, however… Expand
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