Neuronal localization of C1q in preclinical Alzheimer's disease

Complement has been postulated to contribute to inflammatory reactions associated with the neuropathology of Alzheimer's disease (AD). C1q, an initial component of the complement cascade, is associated with neuritic plaques and with neurons in the hippocampus of AD brain. Here, we report the pr...

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Main Authors: Maria I Fonseca, Claudia H Kawas, Juan C Troncoso, Andrea J Tenner
Format: Article
Language:English
Published: Elsevier 2004-02-01
Series:Neurobiology of Disease
Subjects:
Online Access:http://www.sciencedirect.com/science/article/pii/S096999610300189X
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author Maria I Fonseca
Claudia H Kawas
Juan C Troncoso
Andrea J Tenner
author_facet Maria I Fonseca
Claudia H Kawas
Juan C Troncoso
Andrea J Tenner
author_sort Maria I Fonseca
collection DOAJ
description Complement has been postulated to contribute to inflammatory reactions associated with the neuropathology of Alzheimer's disease (AD). C1q, an initial component of the complement cascade, is associated with neuritic plaques and with neurons in the hippocampus of AD brain. Here, we report the presence of C1q in a cognitively intact subject, previously identified as preclinical AD. We compared in detail brain tissue of this preclinical case with a genetically related late-onset AD case. In the AD brain, C1q was typically associated with fibrillar Aβ plaques in frontal cortex and with plaques and neurons in the hippocampus. In the preclinical subject, C1q was abundantly present but it was cell-associated only, being primarily colocalized with neurons in both frontal cortex and hippocampus. However, no predominant cortical neuronal C1q localization was found in other preclinical cases or in Down's cases of different ages. Thus, it is possible that this neuronal-associated C1q reflects an early, but transient, response to injury that may modulate the progression of neurological dysfunction in AD.
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spelling doaj.art-c74d7e7f23cc488aba43663903ea82202022-12-21T21:57:46ZengElsevierNeurobiology of Disease1095-953X2004-02-011514046Neuronal localization of C1q in preclinical Alzheimer's diseaseMaria I Fonseca0Claudia H Kawas1Juan C Troncoso2Andrea J Tenner3Department of Molecular Biology and Biochemistry, University of California Irvine, CA, USA; Neurobiology and Behavior and Neurology, University of California, Irvine, CA, USA; Departments of Pathology and Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USADepartment of Molecular Biology and Biochemistry, University of California Irvine, CA, USA; Neurobiology and Behavior and Neurology, University of California, Irvine, CA, USA; Departments of Pathology and Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USADepartment of Molecular Biology and Biochemistry, University of California Irvine, CA, USA; Neurobiology and Behavior and Neurology, University of California, Irvine, CA, USA; Departments of Pathology and Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USADepartment of Molecular Biology and Biochemistry, University of California Irvine, CA, USA; Neurobiology and Behavior and Neurology, University of California, Irvine, CA, USA; Departments of Pathology and Neurology, Johns Hopkins University School of Medicine, Baltimore, MD, USAComplement has been postulated to contribute to inflammatory reactions associated with the neuropathology of Alzheimer's disease (AD). C1q, an initial component of the complement cascade, is associated with neuritic plaques and with neurons in the hippocampus of AD brain. Here, we report the presence of C1q in a cognitively intact subject, previously identified as preclinical AD. We compared in detail brain tissue of this preclinical case with a genetically related late-onset AD case. In the AD brain, C1q was typically associated with fibrillar Aβ plaques in frontal cortex and with plaques and neurons in the hippocampus. In the preclinical subject, C1q was abundantly present but it was cell-associated only, being primarily colocalized with neurons in both frontal cortex and hippocampus. However, no predominant cortical neuronal C1q localization was found in other preclinical cases or in Down's cases of different ages. Thus, it is possible that this neuronal-associated C1q reflects an early, but transient, response to injury that may modulate the progression of neurological dysfunction in AD.http://www.sciencedirect.com/science/article/pii/S096999610300189XC1qComplementInflammationAlzheimer's diseaseNeurons
spellingShingle Maria I Fonseca
Claudia H Kawas
Juan C Troncoso
Andrea J Tenner
Neuronal localization of C1q in preclinical Alzheimer's disease
Neurobiology of Disease
C1q
Complement
Inflammation
Alzheimer's disease
Neurons
title Neuronal localization of C1q in preclinical Alzheimer's disease
title_full Neuronal localization of C1q in preclinical Alzheimer's disease
title_fullStr Neuronal localization of C1q in preclinical Alzheimer's disease
title_full_unstemmed Neuronal localization of C1q in preclinical Alzheimer's disease
title_short Neuronal localization of C1q in preclinical Alzheimer's disease
title_sort neuronal localization of c1q in preclinical alzheimer s disease
topic C1q
Complement
Inflammation
Alzheimer's disease
Neurons
url http://www.sciencedirect.com/science/article/pii/S096999610300189X
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AT claudiahkawas neuronallocalizationofc1qinpreclinicalalzheimersdisease
AT juanctroncoso neuronallocalizationofc1qinpreclinicalalzheimersdisease
AT andreajtenner neuronallocalizationofc1qinpreclinicalalzheimersdisease