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Related Experiment Video

Updated: May 16, 2026

Absolute Quantification of Aβ1-42 in CSF Using a Mass Spectrometric Reference Measurement Procedure
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Published on: March 21, 2017

Quantification of amyloid precursor protein isoforms using quantification concatamer internal standard.

Junjun Chen1, Meiyao Wang, Illarion V Turko

  • 1Institute for Bioscience and Biotechnology Research, Rockville, Maryland 20850, United States.

Analytical Chemistry
|November 29, 2012
PubMed
Summary

Quantifying protein isoforms like amyloid precursor protein (APP) is challenging. A new method using a quantification concatamer (QconCAT) accurately measures APP and amyloid-beta levels in Alzheimer's disease.

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Area of Science:

  • Proteomics
  • Neuroscience
  • Biochemistry

Background:

  • Protein isoforms can indicate early pathological changes.
  • Quantifying specific protein isoforms is difficult due to shared and unique sequences.
  • Quantification concatamer (QconCAT) technology enables large-scale proteome quantification.

Purpose of the Study:

  • To develop a QconCAT for quantifying amyloid precursor protein (APP) isoforms.
  • To enable selective measurement of common and unique APP peptides.
  • To quantify total APP, APP695, and amyloid-beta (Aβ) in Alzheimer's disease.

Main Methods:

  • Developed an isotope-labeled APP-QconCAT incorporating unique and common APP tryptic peptides.
  • Expressed, purified, and characterized the APP-QconCAT.

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  • Utilized APP-QconCAT for quantitative mass spectrometry in human brain tissue.
  • Main Results:

    • Successfully developed and validated an APP-QconCAT.
    • Quantified total APP, APP695, and Aβ levels in control and Alzheimer's disease brain samples.
    • Demonstrated the utility of QconCAT for isoform-specific protein quantification.

    Conclusions:

    • APP-QconCAT is a powerful tool for accurate quantification of APP isoforms.
    • This method advances understanding of APP's role in Alzheimer's pathogenesis.
    • Further application of APP-QconCATs will elucidate biological mechanisms in Alzheimer's disease.