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Brief Communication
Nature Neuroscience  4, 233 - 234 (2001)
doi:10.1038/85064

BACE1 is the major bold beta-secretase for generation of Abold beta peptides by neurons

Huaibin Cai1, Yanshu Wang4, Diane McCarthy6, Hongjin Wen1, David R. Borchelt1, 3, Donald L. Price1, 2, 3, 5 & Philip C. Wong1, 5

1  Department of Pathology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

2  Department of Neurology, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

3  Department of Neuroscience, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

4  Department of Molecular Biology and Genetics, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

5  Program in Cellular and Molecular Medicine, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA

6  Ciphergen Biosystems, Fremont, California 94555, USA

Correspondence should be addressed to Philip C. Wong wong@jhmi.edu
Two beta-secretases, BACE1 and BACE2, are involved in generation of Alzheimer's disease Abeta peptides1, 2, 3. We report that secretion of Abeta peptides (Abeta1−40/42 and Abeta11−40/42) is abolished in cultures of BACE1-deficient embryonic cortical neurons, and that whereas both human and murine BACE1 can cleave either human or murine beta-amyloid precursor protein (APP) at the +1 site of Abeta, cleavage at the +11 site is species specific. We establish that BACE1 is the principal neuronal protease required to cleave APP at +1 and +11 sites that generate N-termini of Abeta.


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Nature Neuroscience
ISSN: 1097-6256
EISSN: 1546-1726
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