The normal and pathologic roles of the Alzheimer's β-secretase, BACE1

Patty C. Kandalepas, Robert Vassar*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

33 Scopus citations

Abstract

As the most common neurodegenerative disease, therapeutic avenues for the treatment and prevention of Alzheimer's Disease are highly sought after. The aspartic protease BACE1 is the initiator enzyme for the formation of Aβ, a major constituent of amyloid plaques that represent one of the hallmark pathological features of this disorder. Thus, targeting BACE1 for disease-modifying AD therapies represents a rationale approach. The collective knowledge acquired from investigations of BACE1 deletion mutants and characterization of BACE1 substrates has downstream significance not only for the discovery of AD drug therapies but also for predicting side effects of BACE1 inhibition. Here we discuss the identification and validation of BACE1 as the β-secretase implicated in AD, in addition to information regarding BACE1 cell biology, localization, substrates and potential physiological functions derived from BACE1 knockout models.

Original languageEnglish (US)
Pages (from-to)441-449
Number of pages9
JournalCurrent Alzheimer Research
Volume11
Issue number5
DOIs
StatePublished - 2014

Keywords

  • Alzheimer's disease
  • BACE1
  • Beta-secretase

ASJC Scopus subject areas

  • Neurology
  • Clinical Neurology

Fingerprint

Dive into the research topics of 'The normal and pathologic roles of the Alzheimer's β-secretase, BACE1'. Together they form a unique fingerprint.

Cite this