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Related Experiment Videos

Complement C1-inhibitor expression in Alzheimer's disease

R Veerhuis1, I Janssen, J J Hoozemans

  • 1Department of Psychiatry, Research Institute Neurosciences Vrije Universiteit, Graduate School Neurosciences Amsterdam, The Netherlands. r.veerhuis@azvu.nl

Acta Neuropathologica
|October 1, 1998
PubMed
Summary
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Alzheimer's disease involves complement system activation. Astrocytes and neuroblastoma cells secrete C1-esterase inhibitor (C1-Inh), but only interferon-gamma (IFN-gamma) stimulates this. Neurons may produce C1-Inh in vivo.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Complement system activation is implicated in Alzheimer's disease (AD) pathogenesis.
  • C1-esterase inhibitor (C1-Inh), a complement regulator, is found in AD brain lesions.
  • The cellular source and regulation of C1-Inh in AD remain unclear.

Purpose of the Study:

  • To identify the cellular source of C1-esterase inhibitor (C1-Inh) in the brain.
  • To investigate the regulation of C1-Inh secretion by cytokines relevant to AD.
  • To explore the role of neurons and astrocytes in C1-Inh production in vivo and in vitro.

Main Methods:

  • Primary astrocyte and neuroblastoma cell cultures.
  • Measurement of C1-Inh protein secretion.
  • Stimulation with recombinant human interferon-gamma (IFN-gamma), interleukin (IL)-1beta, IL-6, and tumor necrosis factor (TNF)-alpha.

Related Experiment Videos

  • In situ hybridization for C1-Inh mRNA expression.

    • Main Results:

    • Astrocytes and neuroblastoma cell lines secrete active C1-Inh.
    • IFN-gamma significantly stimulated C1-Inh secretion by astrocytes and one neuroblastoma cell line.
    • Other AD-associated cytokines (IL-1beta, IL-6, TNF-alpha) did not stimulate C1-Inh secretion.
    • In situ hybridization indicated neurons, not astrocytes, express C1-Inh mRNA in vivo.

    Conclusions:

    • Astrocytes and neuroblastoma cells are sources of secreted C1-Inh.
    • IFN-gamma is a potent stimulator of C1-Inh secretion, while other AD-related cytokines are not.
    • Neurons are likely producers of C1-Inh in the brain parenchyma.
    • The in vivo stimulus for neuronal C1-Inh expression in AD requires further investigation.