Alterations in behavior, amyloid beta-42, caspase-3, and Cox-2 in mutant PS2 transgenic mouse model of Alzheimer's disease.

@article{Hwang2002AlterationsIB,
  title={Alterations in behavior, amyloid beta-42, caspase-3, and Cox-2 in mutant PS2 transgenic mouse model of Alzheimer's disease.},
  author={Dae Youn Hwang and Kab Ryong Chae and Tae Seok Kang and Jin Hee Hwang and Chae Hyung Lim and Hyun Ki Kang and Jun Seo Goo and Mi Ra Lee and Hwa Ja Lim and Sae H. Min and Jun Yong Cho and Jin Tae Hong and Chi Won Song and Sang Gi Paik and Jung Cho and Yong Kyu Kim},
  journal={FASEB journal : official publication of the Federation of American Societies for Experimental Biology},
  year={2002},
  volume={16 8},
  pages={805-13}
}
Alzheimer's disease (AD) occurs when neurons in the memory and cognition regions of the brain are accompanied by an accumulation of the long amyloid beta-proteins of the 39 to 43 amino acids derived from the amyloid precursor protein (APP) by cleavage with beta- and gamma-secretase. An increased production of Abeta-42 by mutation of PS2 genes promotes caspase expression and is associated with the Cox-2 found in the brain of AD patients. To address this question in vivo, we expressed the human… CONTINUE READING

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