Cookies on this website
We use cookies to ensure that we give you the best experience on our website. If you click 'Continue' we'll assume that you are happy to receive all cookies and you won't see this message again. Click 'Find out more' for information on how to change your cookie settings.

The beta-site of beta-amyloid precursor protein cleaving enzyme (BACE) cleaves the beta-amyloid (Abeta) precursor protein at the N-terminal end of Abeta, allowing for the production of Abeta by C-terminal gamma-secretase cleavage. We hypothesized that over-activity of BACE might lead to the overproduction of Abeta, 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 publication

DOI

10.1016/s0304-3940(01)02234-0

Type

Journal article

Journal

Neuroscience letters

Publication Date

11/2001

Volume

313

Pages

105 - 107

Addresses

Department of Molecular Genetics, Flanders Interuniversity Institute for Biotechnology, University of Antwerp, Universiteitsplein 1, B-2018 Antwerp, Belgium.

Keywords

Humans, Alzheimer Disease, Endopeptidases, Amyloid beta-Protein Precursor, Age of Onset, Genotype, Genes, Dominant, Polymorphism, Genetic, Middle Aged, Amyloid Precursor Protein Secretases, Aspartic Acid Endopeptidases, Genetic Linkage