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The Journal of Neuroscience, October 14, 2009, 29(41):12787-12794; doi:10.1523/JNEUROSCI.3657-09.2009

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Symposia and Mini-Symposia
The β-Secretase Enzyme BACE in Health and Alzheimer's Disease: Regulation, Cell Biology, Function, and Therapeutic Potential

Robert Vassar,¹ Dora M. Kovacs,² Riqiang Yan,³ and Philip C. Wong⁴

¹Department of Cell and Molecular Biology, Northwestern University, Chicago, Illinois 60611, ²MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital and Department of Neurology, Harvard Medical School, Charlestown, Massachusetts 02129, ³Department of Neuroscience, Cleveland Clinic, Lerner Research Institute, Cleveland, Ohio 44195, and ⁴Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland 21231

Correspondence should be addressed to Robert Vassar at the above address. Email: r-vassar{at}northwestern.edu

The β-amyloid (Aβ) peptide is the major constituent of amyloid plaques in Alzheimer's disease (AD) brain and is likely to play a central role in the pathogenesis of this devastating neurodegenerative disorder. The β-secretase, β-site amyloid precursor protein cleaving enzyme (BACE1; also called Asp2, memapsin 2), is the enzyme responsible for initiating Aβ generation. Thus, BACE is a prime drug target for the therapeutic inhibition of Aβ production in AD. Since its discovery 10 years ago, much has been learned about BACE. This review summarizes BACE properties, describes BACE translation dysregulation in AD, and discusses BACE physiological functions in sodium current, synaptic transmission, myelination, and schizophrenia. The therapeutic potential of BACE will also be considered. This is a summary of topics covered at a symposium held at the 39th annual meeting of the Society for Neuroscience and is not meant to be a comprehensive review of BACE.

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Received July 28, 2009; revised Aug. 27, 2009; accepted Aug. 28, 2009.

Correspondence should be addressed to Robert Vassar at the above address. Email: r-vassar{at}northwestern.edu

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