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 Citations (Scopus)

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
StatePublished - Jan 1 2003

Fingerprint

Calreticulin
Alzheimer Disease
Reactive Oxygen Species
Neurons
Oxidative Stress
Modern 1601-history
Neurotoxins
Brain Diseases
Amyloid
Fluorescent Antibody Technique
Binding Sites
Antibodies
Wounds and Injuries

Keywords

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

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Neurology
  • Clinical Neurology

Cite this

C1q-calreticulin induced oxidative neurotoxicity : Relevance for the neuropathogenesis of Alzheimer's disease. / Luo, Xiaoguang; Weber, Gregory A.; Zheng, Jialin C; Gendelman, Howard Eliot; Ikezu, Tsuneya.

In: Journal of Neuroimmunology, Vol. 135, No. 1-2, 01.01.2003, p. 62-71.

Research output: Contribution to journalArticle

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