The β-secretase enzyme BACE in health and Alzheimer's disease: Regulation, cell biology, function, and therapeutic potential

Robert Vassar, Dora M. Kovacs, Riqiang Yan, Philip C. Wong

Research output: Contribution to journalArticle

Abstract

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.

Original languageEnglish (US)
Pages (from-to)12787-12794
Number of pages8
JournalJournal of Neuroscience
Volume29
Issue number41
DOIs
StatePublished - Oct 14 2009

    Fingerprint

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this