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 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 Abeta 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.
Fonseca
Maria I
MI
Department of Molecular Biology and Biochemistry, University of California, Irvine, CA 92697, USA.
Kawas
Claudia H
CH
Troncoso
Juan C
JC
Tenner
Andrea J
AJ
D000328:Adult; D000368:Aged; D000544:Alzheimer Disease / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D016229:Amyloid beta-Peptides / Q000276:immunology / Q000378:metabolism; D052160:Benzothiazoles; D015415:Biomarkers; D001921:Brain / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D002540:Cerebral Cortex / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D015922:Complement C1q / Q000276:immunology* / Q000378:metabolism; D018450:Disease Progression; D004314:Down Syndrome / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D004660:Encephalitis / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D005260:Female; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005904:Glial Fibrillary Acidic Protein / Q000276:immunology / Q000378:metabolism; D005911:Gliosis / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006624:Hippocampus / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007150:Immunohistochemistry; D008875:Middle Aged; D009474:Neurons / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D010446:Peptide Fragments / Q000276:immunology / Q000378:metabolism; D058225:Plaque, Amyloid / Q000276:immunology / Q000378:metabolism / Q000473:pathology; D013844:Thiazoles
D016229:Amyloid beta-Peptides; D052160:Benzothiazoles; D015415:Biomarkers; D005904:Glial Fibrillary Acidic Protein; D010446:Peptide Fragments; D013844:Thiazoles; C075222:amyloid beta-protein (1-42); C009462:thioflavin T; D015922:Complement C1q