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Related Experiment Videos

APP gene family. Alternative splicing generates functionally related isoforms

R Sandbrink1, C L Masters, K Beyreuther

  • 1Zentrum für Molekulare Biologie Heidelberg (ZMBH), University of Heidelberg, Germany.

Annals of the New York Academy of Sciences
|January 17, 1996
PubMed
Summary
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Alternative splicing of Alzheimer's beta A4-amyloid protein precursor (APP) and APP-like proteins (APLPs) influences their function and expression in neurons. This may explain neuron vulnerability in Alzheimer's disease.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Biochemistry

Background:

  • Alzheimer's beta A4-amyloid protein precursor (APP) and APP-like proteins (APLPs) share structural similarities and are involved in neuronal function.
  • Alternative splicing generates diverse APP and APLP isoforms with distinct expression patterns in rat tissues and neurons.

Purpose of the Study:

  • To investigate the functional implications of alternative splicing in APP and APLP2, focusing on divergent domains and their impact on protein function.
  • To explore how these splicing events may contribute to the selective vulnerability of neurons in Alzheimer's disease.

Main Methods:

  • Analysis of alternative splicing patterns in APP and APLP2 mRNA transcripts.
  • Examination of structural similarities in divergent domains of APP and APLP2 isoforms.

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  • Prediction of secondary structures and functional sites, such as glycosaminoglycan attachment sites.

    • Main Results:

    • Specific alternatively spliced isoforms of APP (lacking exon 15) and APLP2 (lacking the 12 aa exon) show distinct tissue expression patterns.
    • Structural similarities were found in the divergent domains of APP and APLP2, suggesting related functions.
    • A chondroitin sulfate glycosaminoglycan attachment site is present in L-APP and L-APLP2 but interrupted in isoforms with exon 15 or the 12 aa exon, respectively.

    Conclusions:

    • Alternative splicing of APP and APLP2 regulates binding properties and potentially beta-secretase cleavage, influencing beta A4-protein liberation.
    • The low expression of L-APP and high APP content in neurons may render them susceptible to beta A4-protein accumulation, contributing to Alzheimer's disease pathogenesis.