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Expression of amyloid beta-protein precursor mRNAs in familial Alzheimer's disease

P J Harrison1, A J Barton, R C Pearson

  • 1Department of Anatomy, St. Mary's Hospital Medical School, London, UK.

Neuroreport
|March 1, 1991
PubMed

Insights

This study investigated amyloid beta-protein precursor (APP) gene expression in familial Alzheimer's disease (FAD) brains. Researchers found no differences in APP transcript levels, suggesting overexpression isn't the cause of beta-amyloid peptide deposition.

Area of Science:

  • Neuroscience
  • Genetics
  • Pathology

Background:

  • Alzheimer's disease (AD) pathogenesis involves the amyloid beta-protein precursor (APP) gene and its products.
  • Differential expression of APP transcripts is a potential factor in AD development.

Purpose of the Study:

  • To investigate the distribution and quantity of messenger RNAs (mRNAs) encoding APP variants in familial Alzheimer's disease (FAD) brains.
  • To determine if altered APP mRNA levels contribute to beta-amyloid (beta/A4) peptide deposition in FAD.

Main Methods:

  • In-situ hybridization histochemistry was employed to analyze APP transcript distribution.
  • Brain tissue from three FAD cases and control subjects was examined.

Main Results:

  • No significant differences in the distribution or quantity of APP transcripts were observed between FAD cases and control groups.
  • One FAD case featured a mutation within the APP gene, but this did not alter overall transcript distribution patterns.

Conclusions:

  • Overexpression of APP mRNAs is unlikely to be the primary cause of beta-amyloid peptide deposition in FAD brains.
  • The findings suggest that other mechanisms may be responsible for beta-amyloid accumulation in familial Alzheimer's disease.

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