Amyloid β secretase gene (BACE) is neither mutated in nor associated with early-onset Alzheimer's disease

Marc Cruts, Bart Dermaut, Rosa Rademakers, Gerwin Roks, Marleen Van den Broeck, Gabriela Munteanu, Cornelia M. Van Duijn, Christine Van Broeckhoven

Research output: Contribution to journalArticle

35 Scopus citations

Abstract

The beta-site of β-amyloid precursor protein cleaving enzyme (BACE) cleaves the β-amyloid (Aβ) precursor protein at the N-terminal end of Aβ, allowing for the production of Aβ by C-terminal γ-secretase cleavage. We hypothesized that over-activity of BACE might lead to the overproduction of Aβ, hence causing Alzheimer's disease (AD). Molecular genetic analyses of BACE in 9 autosomal dominant AD families and a population-based sample of 101 presenile AD cases did not identify genetic linkage, pathogenic mutations or genetic association with BACE, suggesting that BACE is not genetically involved in the etiology of AD.

Original languageEnglish (US)
Pages (from-to)105-107
Number of pages3
JournalNeuroscience Letters
Volume313
Issue number1-2
DOIs
StatePublished - Nov 2 2001

Keywords

  • Alzheimer's disease
  • BACE
  • β-amyloid

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Amyloid β secretase gene (BACE) is neither mutated in nor associated with early-onset Alzheimer's disease'. Together they form a unique fingerprint.

  • Cite this

    Cruts, M., Dermaut, B., Rademakers, R., Roks, G., Van den Broeck, M., Munteanu, G., Van Duijn, C. M., & Van Broeckhoven, C. (2001). Amyloid β secretase gene (BACE) is neither mutated in nor associated with early-onset Alzheimer's disease. Neuroscience Letters, 313(1-2), 105-107. https://doi.org/10.1016/S0304-3940(01)02234-0