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Related Experiment Videos

Complement activation by islet amyloid polypeptide (IAPP) and alpha-synuclein 112.

Andis Klegeris1, Patrick L McGeer

  • 1Kinsmen Laboratory of Neurological Research, University of British Columbia, 2255 Wesbrook Mall, Vancouver, BC, Canada V6T 1Z3.

Biochemical and Biophysical Research Communications
|April 27, 2007
PubMed
Summary

Overactivated complement damages tissues in diseases like Alzheimer's and Parkinson's. This study found islet amyloid polypeptide and a specific alpha-synuclein form activate complement, suggesting new therapeutic targets.

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Area of Science:

  • Immunology
  • Neuroscience
  • Endocrinology

Background:

  • Complement system overactivation can lead to host tissue damage.
  • Evidence suggests complement-mediated self-damage in Alzheimer's disease (AD), age-related macular degeneration, type 1 diabetes mellitus (T1DM), and Parkinson's disease (PD).
  • Amyloid beta (Abeta) and immunoglobulin G (IgG) are known complement activators in AD and T1DM, respectively.

Purpose of the Study:

  • To investigate the complement-activating potential of islet amyloid polypeptide (IAPP) and alpha-synuclein (alpha-Syn).
  • To compare the in vitro complement activation by IAPP and alpha-Syn with known activators like Abeta and IgG.
  • To explore the role of complement activation in type 2 diabetes mellitus (T2DM) and Parkinson's disease (PD).

Main Methods:

Related Experiment Videos

  • In vitro assays were performed to measure complement activation.
  • The complement-activating ability of IAPP and different forms of alpha-Syn was compared.
  • Known complement activators Abeta and IgG served as controls.

    • Main Results:

    • Islet amyloid polypeptide (IAPP) activated complement in vitro.
    • The alternatively spliced alpha-Syn 112 form activated complement, while the full-length alpha-Syn 140 form did not.
    • These findings were observed in comparison to Abeta and IgG.

    Conclusions:

    • Complement activation by IAPP may contribute to the death of insulin-secreting cells in T2DM.
    • Complement activation by alpha-Syn 112 could play a role in neuronal death in PD and related synucleinopathies.
    • Targeting complement activation presents a potential therapeutic strategy for various age-related degenerative diseases.