Journal article

Acetylcholinesterase is increased in the brains of transgenic mice expressing the C-terminal fragment (CT100) of the β-amyloid protein precursor of Alzheimer's disease

G Sberna, J Sáez-Valero, QX Li, C Czech, K Beyreuther, CL Masters, CA McLean, DH Small

Journal of Neurochemistry | WILEY | Published : 1998

Abstract

Acetylcholinesterase (AChE) expression is markedly affected in Alzheimer's disease (AD). AChE activity is lower in most regions of the AD brain, but it is increased within and around amyloid plaques. We have previously shown that AChE expression in P19 cells is increased by the amyloid β protein (Aβ). The aim of this study was to investigate AChE expression using a transgenic mouse model of Aβ overproduction. The β- actin promoter was used to drive expression of a transgene encoding the 100- amino acid C-terminal fragment of the human amyloid precursor protein (APP CT100). Analysis of extracts from transgenic mice revealed that the human sequences of full-length human APP CT100 and Aβ were o..

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University of Melbourne Researchers