1991NeuroreportRequires access

Expression of amyloid beta-protein precursor mRNAs in familial Alzheimerʼs disease

Paul J. Harrison, A.J.L. Barton, R.C.A. Pearson

Open publisher page 5 citations

Abstract

The amyloid beta-protein precursor (APP) gene and its products are implicated in the pathogenesis of Alzheimer's disease. The differential expression of APP transcripts may contribute to this process. In the present study, the distribution of mRNAs encoding APP variants has been determined in the brain of three cases of familial Alzheimer's disease (FAD) using in-situ hybridization histochemistry. One FAD case was associated with a mutation in the APP gene. No differences in distribution or quantity of APP transcripts were observed between FAD cases and controls. Overexpression of APP mRNAs is therefore an unlikely explanation for the deposition of the beta-amyloid (beta/A4) peptide in FAD brains.

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What this paper is about

The amyloid beta-protein precursor (APP) gene and its products are implicated in the pathogenesis of Alzheimer's disease. The differential expression of APP transcripts may contribute to this process. In the present study, the distribution of mRNAs encoding APP variants has been determined in the brain of three cases of familial Alzheimer's disease (FAD) using in-situ hybridization histochemistry. One FAD case was associated with a mutation in the APP gene. No differences in distribution or quantity of APP transcripts were observed between FAD cases and controls. Overexpression of APP mRNAs is therefore an unlikely explanation for the deposition of the beta-amyloid (beta/A4) peptide in FAD brains.

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Available abstract

The amyloid beta-protein precursor (APP) gene and its products are implicated in the pathogenesis of Alzheimer's disease. The differential expression of APP transcripts may contribute to this process. In the present study, the distribution of mRNAs encoding APP variants has been determined in the brain of three cases of familial Alzheimer's disease (FAD) using in-situ hybridization histochemistry. One FAD case was associated with a mutation in the APP gene. No differences in distribution or quantity of APP transcripts were observed between FAD cases and controls. Overexpression of APP mRNAs is therefore an unlikely explanation for the deposition of the beta-amyloid (beta/A4) peptide in FAD brains.

Key concepts: Amyloid precursor protein, BACE1-AS, Pathogenesis, Alzheimer's disease, In situ hybridization, Amyloid (mycology), BETA (programming language), Gene expression

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