Journal
CELLULAR AND MOLECULAR LIFE SCIENCES
Volume 65, Issue 20, Pages 3265-3289Publisher
SPRINGER BASEL AG
DOI: 10.1007/s00018-008-8271-3
Keywords
Alzheimer's disease; BACE1; aspartic protease; amyloid-beta; neurodegeneration
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Funding
- Higher Education Authority Government of Ireland Programme for Research in Third Levels Institutions (HEA-PRTLI3)
- Health Research Board of Ireland
- Science Foundation Ireland
- Research Frontiers Programme
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The identification of the aspartic protease BACE1 (beta-secretase) was a defining event in research aimed at understanding the molecular mechanisms that underlie Alzheimer's disease (AD) pathogenesis. This is because BACE1 catalyses the rate limiting step in the production of amyloid-beta (A beta) the principal component of plaque pathology in AD, the excessive production of which is believed to be a primary cause of neurodegeneration, and cognitive dysfunction in AD. Subsequent discoveries showed that genetic deletion of BACE1 completely abolishes A beta production and deposition in vivo, and that BACE1 activity is significantly increased in AD brain. In this review we present current knowledge on BACE1, discussing its structure, function and complex regulation with a view to understanding BACE1 function in the brain, and BACE1 as a target in blocking aberrant A beta production in AD.
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