Increased fibrillar β-amyloid in response to human C1q injections into hippocampus and cortex of APP+PS1 transgenic mice

Kristal W. Boyett, Giovanni DiCarlo, Paul T. Jantzen, Jennifer Jackson, Charlotte O'Leary, Donna Wilcock, Dave Morgan, Marcia N. Gordon

Research output: Contribution to journalArticlepeer-review

29 Scopus citations


Human C1q when injected directly into hippocampus and cortex of doubly transgenic APP+PS1 mice results in the increase of Congo red-positive fibrillar deposits. Although there was no significant change in overall area stained for Aβ total, qualitatively it appeared that there was less diffuse Aβ in C1q-treated mice versus vehicle. There was no apparent change in astroglial or microglial activation caused by injection of C1q with respect to vehicle injections. These effects of C1q were only found in 50% BUB/BnJ mice, a strain with higher serum complement activity than other mouse lines. These in vivo data were consistent with the effects of C1q to increase fibrillogenesis of Aβ in vitro. In conclusion, complement protein C1q, believed to be involved in the pathogenesis of Alzheimer's disease in humans, can cause increased fibrillogenesis in the APP+PS1 mouse model of amyloid deposition.

Original languageEnglish
Pages (from-to)83-93
Number of pages11
JournalNeurochemical Research
Issue number1
StatePublished - Jan 1 2003

Bibliographical note

Funding Information:
This work was supported by AG15490 and by the Benjamin Trust. The authors thank the family of Ms. Dorothy Benjamin for her kind and generous donation to Alzheimer’s Research. Thanks to Dr. Paul Gottschall (U.S.F.) for the generous gift of the Aβ antibody. M. N. G. would like to take this opportunity to express her thanks to Dr. Jean de Vellis for providing valuable postdoctoral experience. Jean was the kindest and most gracious mentor possible. I am pleased to be able to contribute to this tribute to him, however humbly.


  • Alzheimer's disease
  • Astrocytes
  • BUB/BnJ
  • Complement
  • Microglia

ASJC Scopus subject areas

  • Biochemistry
  • Cellular and Molecular Neuroscience


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