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

doi:10.1016/S0304-3940(01)02234-0

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

Neuroscience

Research output: Contribution to journal › Article › peer-review

37 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 language	English (US)
Pages (from-to)	105-107
Number of pages	3
Journal	Neuroscience Letters
Volume	313
Issue number	1-2
DOIs	https://doi.org/10.1016/S0304-3940(01)02234-0
State	Published - Nov 2 2001

Keywords

Alzheimer's disease
BACE
β-amyloid

ASJC Scopus subject areas

General Neuroscience

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10.1016/S0304-3940(01)02234-0

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

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.",

keywords = "Alzheimer's disease, BACE, β-amyloid",

author = "Marc Cruts and Bart Dermaut and Rosa Rademakers and Gerwin Roks and {Van den Broeck}, Marleen and Gabriela Munteanu and {Van Duijn}, {Cornelia M.} and {Van Broeckhoven}, Christine",

note = "Funding Information: This work was in part funded by the Fund for Scientific Research–Flanders, Belgium (FWO-F), a special project of the University of Antwerp and a grant of the Netherlands Organization of Scientific Research (NWO). Marc Cruts is a postdoctoral fellow, and Bart Dermaut and Rosa Rademakers are Ph.D. fellows of the FWO.",

year = "2001",

month = nov,

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doi = "10.1016/S0304-3940(01)02234-0",

language = "English (US)",

volume = "313",

pages = "105--107",

journal = "Neuroscience Letters",

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publisher = "Elsevier Ireland Ltd",

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T1 - Amyloid β secretase gene (BACE) is neither mutated in nor associated with early-onset Alzheimer's disease

AU - Cruts, Marc

AU - Dermaut, Bart

AU - Rademakers, Rosa

AU - Roks, Gerwin

AU - Van den Broeck, Marleen

AU - Munteanu, Gabriela

AU - Van Duijn, Cornelia M.

AU - Van Broeckhoven, Christine

N1 - Funding Information: This work was in part funded by the Fund for Scientific Research–Flanders, Belgium (FWO-F), a special project of the University of Antwerp and a grant of the Netherlands Organization of Scientific Research (NWO). Marc Cruts is a postdoctoral fellow, and Bart Dermaut and Rosa Rademakers are Ph.D. fellows of the FWO.

PY - 2001/11/2

Y1 - 2001/11/2

N2 - 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.

AB - 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.

KW - Alzheimer's disease

KW - BACE

KW - β-amyloid

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U2 - 10.1016/S0304-3940(01)02234-0

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SN - 0304-3940

VL - 313

SP - 105

EP - 107

JO - Neuroscience Letters

JF - Neuroscience Letters

IS - 1-2

ER -

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

Abstract

Keywords

ASJC Scopus subject areas

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