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

doi:10.1023/A:1021600212829

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 journal › Article › peer-review

29 Scopus citations

Abstract

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 language	English
Pages (from-to)	83-93
Number of pages	11
Journal	Neurochemical Research
Volume	28
Issue number	1
DOIs	https://doi.org/10.1023/A:1021600212829
State	Published - 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.

Funding

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.

Funders	Funder number
National Institute on Aging	R01AG015490

Keywords

Alzheimer's disease
Astrocytes
BUB/BnJ
Complement
Microglia

ASJC Scopus subject areas

Biochemistry
Cellular and Molecular Neuroscience

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

Access to Document

10.1023/A:1021600212829

Cite this

@article{27d95f1db32146589e56d7c175ae7a35,

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

abstract = "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.",

keywords = "Alzheimer's disease, Astrocytes, BUB/BnJ, Complement, Microglia",

author = "Boyett, {Kristal W.} and Giovanni DiCarlo and Jantzen, {Paul T.} and Jennifer Jackson and Charlotte O'Leary and Donna Wilcock and Dave Morgan and Gordon, {Marcia N.}",

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{\textquoteright}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.",

year = "2003",

month = jan,

day = "1",

doi = "10.1023/A:1021600212829",

language = "English",

volume = "28",

pages = "83--93",

number = "1",

}

TY - JOUR

T1 - Increased fibrillar β-amyloid in response to human C1q injections into hippocampus and cortex of APP+PS1 transgenic mice

AU - Boyett, Kristal W.

AU - DiCarlo, Giovanni

AU - Jantzen, Paul T.

AU - Jackson, Jennifer

AU - O'Leary, Charlotte

AU - Wilcock, Donna

AU - Morgan, Dave

AU - Gordon, Marcia N.

N1 - 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.

PY - 2003/1/1

Y1 - 2003/1/1

N2 - 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.

AB - 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.

KW - Alzheimer's disease

KW - Astrocytes

KW - BUB/BnJ

KW - Complement

KW - Microglia

UR - http://www.scopus.com/inward/record.url?scp=0037267982&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0037267982&partnerID=8YFLogxK

U2 - 10.1023/A:1021600212829

DO - 10.1023/A:1021600212829

M3 - Article

C2 - 12587666

AN - SCOPUS:0037267982

SN - 0364-3190

VL - 28

SP - 83

EP - 93

JO - Neurochemical Research

JF - Neurochemical Research

IS - 1

ER -

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

Abstract

Bibliographical note

Funding

Keywords

ASJC Scopus subject areas

UN SDGs

Access to Document

Other files and links

Fingerprint

Cite this