C1q-calreticulin induced oxidative neurotoxicity: Relevance for the neuropathogenesis of Alzheimer's disease

Xiaoguang Luo, Gregory A. Weber, Jialin C Zheng, Howard Eliot Gendelman, Tsuneya Ikezu

Research output: Contribution to journalArticle

42 Scopus citations

Abstract

Alzheimer's disease (AD) remains one of the most challenging brain disorders facing modern medicine. Neuronal loss underlies the pathogenesis of AD and can occur, in part, by oxidative stress, by β-amyloid peptide (Aβ), and by excitotoxins. The complement cascade, especially C1q, may affect reactive oxygen species (ROS) and mediate neuronal injury during AD. We demonstrate that incubation of neurons with purified C1q results in increased ROS, which can be partially blocked by low concentrations of Aβ. C1q-binding sites on neurons were demonstrated by 125I-C1q-binding and immunofluorescence tests performed on primary neurons. The blocking of neuronal calreticulin by its antibody abrogated ROS by C1q. We suggest that the C1q may be an important factor contributing to neuronal oxidative stress and neuronal demise during AD.

Original languageEnglish (US)
Pages (from-to)62-71
Number of pages10
JournalJournal of Neuroimmunology
Volume135
Issue number1-2
DOIs
Publication statusPublished - Feb 2003

    Fingerprint

Keywords

  • C1q
  • Calreticulin
  • Neurons
  • Reactive oxygen species
  • β-Amyloid peptide

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Cite this