Beta-secretase-1 elevation in transgenic mouse models of Alzheimer's disease is associated with synaptic/axonal pathology and amyloidogenesis: implications for neuritic plaque development.

@article{Zhang2009Betasecretase1EI,
  title={Beta-secretase-1 elevation in transgenic mouse models of Alzheimer's disease is associated with synaptic/axonal pathology and amyloidogenesis: implications for neuritic plaque development.},
  author={Xuemei Zhang and Yan Cai and Kun Xiong and Huaibin Cai and Xue-gang Luo and Jia-Chun Feng and Richard W. Clough and Robert G. Struble and Peter R Patrylo and Xiaoxin Yan},
  journal={The European journal of neuroscience},
  year={2009},
  volume={30 12},
  pages={2271-83}
}
The presence of neuritic plaques is a pathological hallmark of Alzheimer's disease (AD). However, the origin of extracellular beta-amyloid peptide (Abeta) deposits and the process of plaque development remain poorly understood. The present study attempted to explore plaque pathogenesis by localizing beta-secretase-1 (BACE1) elevation relative to Abeta accumulation and synaptic/neuritic alterations in the forebrain, using transgenic mice harboring familial AD (FAD) mutations (5XFAD and 2XFAD) as… CONTINUE READING