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Nature Medicine 9, 3 - 4 (2003)
doi:10.1038/nm0103-3

Elevated bold beta-secretase expression and enzymatic activity detected in sporadic Alzheimer disease

Li-Bang Yang1, Kristina Lindholm1, Riqiang Yan4, Martin Citron5, Weiming Xia6, Xiao-Li Yang1, Thomas Beach2, Lucia Sue2, Philip Wong7, Donald Price7, Rena Li3 & Yong Shen1

  1. Haldeman Laboratory of Molecular and Cellular Neurobiology, Sun City, Arizona, USA
  2. Brain Bank and Civin Neuropathology Laboratory Sun City, Arizona, USA
  3. L.J. Roberts Center for Alzheimer's Research, Sun Health Research Institute, Sun City, Arizona, USA
  4. Department of Cell and Molecular Biology, Pharmacia Corp., Kalamazoo, Michigan, USA
  5. Department of Neuroscience, Amgen, Inc., Thousands Oaks, California, USA
  6. Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts, USA
  7. Department of Pathology, Laboratory of Neuropathology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA

Correspondence to: Yong Shen1 e-mail: yong.shen@sunhealth.org

A critical feature of Alzheimer disease (AD) is the deposition of plaque, which contains high levels of amyloid-beta (Abeta) peptides1. A small subset of AD patients carry the Swedish mutation2, 3 in the amyloid precursor protein (APP) gene, selectively increasing beta-secretase (BACE) cleavage products, of which subsequent cleavage by gamma-secretase leads to Abeta formation.

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