Analysis of the Putative Role of CR1 in Alzheimer's Disease: Genetic Association, Expression and Function
Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). Recent large genome wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) in the C3b/C4b receptor (CR1 or CD35) that are associat...
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Published in | PloS one Vol. 11; no. 2; p. e0149792 |
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Main Authors | , , , , , , , , , |
Format | Journal Article |
Language | English |
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United States
Public Library of Science
25.02.2016
Public Library of Science (PLoS) |
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Abstract | Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). Recent large genome wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) in the C3b/C4b receptor (CR1 or CD35) that are associated with late onset AD. Here, anti-CR1 antibodies (Abs) directed against different epitopes of the receptor, were used to localize CR1 in brain, and relative binding affinities of the CR1 ligands, C1q and C3b, were assessed by ELISA. Most Abs tested stained red blood cells in blood vessels but showed no staining in brain parenchyma. However, two monoclonal anti-CR1 Abs labeled astrocytes in all of the cases tested, and this reactivity was preabsorbed by purified recombinant human CR1. Human brain-derived astrocyte cultures were also reactive with both mAbs. The amount of astrocyte staining varied among the samples, but no consistent difference was conferred by diagnosis or the GWAS-identified SNPs rs4844609 or rs6656401. Plasma levels of soluble CR1 did not correlate with diagnosis but a slight increase was observed with rs4844609 and rs6656401 SNP. There was also a modest but statistically significant increase in relative binding activity of C1q to CR1 with the rs4844609 SNP compared to CR1 without the SNP, and of C3b to CR1 in the CR1 genotypes containing the rs6656401 SNP (also associated with the larger isoform of CR1) regardless of clinical diagnosis. These results suggest that it is unlikely that astrocyte CR1 expression levels or C1q or C3b binding activity are the cause of the GWAS identified association of CR1 variants with AD. Further careful functional studies are needed to determine if the variant-dictated number of CR1 expressed on red blood cells contributes to the role of this receptor in the progression of AD, or if another mechanism is involved. |
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AbstractList | Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). Recent large genome wide association studies (GWAS) have identified single nucleotide polymorphisms (SNPs) in the C3b/C4b receptor (CR1 or CD35) that are associated with late onset AD. Here, anti-CR1 antibodies (Abs) directed against different epitopes of the receptor, were used to localize CR1 in brain, and relative binding affinities of the CR1 ligands, C1q and C3b, were assessed by ELISA. Most Abs tested stained red blood cells in blood vessels but showed no staining in brain parenchyma. However, two monoclonal anti-CR1 Abs labeled astrocytes in all of the cases tested, and this reactivity was preabsorbed by purified recombinant human CR1. Human brain-derived astrocyte cultures were also reactive with both mAbs. The amount of astrocyte staining varied among the samples, but no consistent difference was conferred by diagnosis or the GWAS-identified SNPs rs4844609 or rs6656401. Plasma levels of soluble CR1 did not correlate with diagnosis but a slight increase was observed with rs4844609 and rs6656401 SNP. There was also a modest but statistically significant increase in relative binding activity of C1q to CR1 with the rs4844609 SNP compared to CR1 without the SNP, and of C3b to CR1 in the CR1 genotypes containing the rs6656401 SNP (also associated with the larger isoform of CR1) regardless of clinical diagnosis. These results suggest that it is unlikely that astrocyte CR1 expression levels or C1q or C3b binding activity are the cause of the GWAS identified association of CR1 variants with AD. Further careful functional studies are needed to determine if the variant-dictated number of CR1 expressed on red blood cells contributes to the role of this receptor in the progression of AD, or if another mechanism is involved. |
Audience | Academic |
Author | Atkinson, John P Brubaker, William D Mastroeni, Diego Chu, Shuhui Hauhart, Richard E Tenner, Andrea J Fonseca, Maria I Rogers, Joseph Clarke, Elizabeth V Pierce, Aimee L |
AuthorAffiliation | 7 School for Mental Health and Neuroscience (MHeNS), Department of Psychiatry and Neuropsychology, Faculty of Health, Medicine and Life Sciences, European Graduate School of Neuroscience (EURON), Maastricht University Medical Centre, Maastricht, The Netherlands 6 Banner Sun Health Research Institute, Sun City, Arizona, 85351, United States of America 4 SRI International, Menlo Park, California, 94025, United States of America 3 UCI Institute for Memory Impairment and Neurological Disorders, University of California Irvine, Irvine, California, 92697, United States of America 5 Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, 63110, United States of America 1 Department of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California, 92697, United States of America 2 Department of Neurology, University of California Irvine, Irvine, California, 92697, United States of America Colorado State University, Col |
AuthorAffiliation_xml | – name: 6 Banner Sun Health Research Institute, Sun City, Arizona, 85351, United States of America – name: 5 Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, 63110, United States of America – name: 7 School for Mental Health and Neuroscience (MHeNS), Department of Psychiatry and Neuropsychology, Faculty of Health, Medicine and Life Sciences, European Graduate School of Neuroscience (EURON), Maastricht University Medical Centre, Maastricht, The Netherlands – name: 8 Department of Neurobiology and Behavior and Department of Pathology and Laboratory Science, University of California Irvine, Irvine, California, 92697, United States of America – name: Colorado State University, College of Veterinary Medicine and Biomedical Sciences, UNITED STATES – name: 3 UCI Institute for Memory Impairment and Neurological Disorders, University of California Irvine, Irvine, California, 92697, United States of America – name: 4 SRI International, Menlo Park, California, 94025, United States of America – name: 1 Department of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California, 92697, United States of America – name: 2 Department of Neurology, University of California Irvine, Irvine, California, 92697, United States of America |
Author_xml | – sequence: 1 givenname: Maria I surname: Fonseca fullname: Fonseca, Maria I organization: Department of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California, 92697, United States of America – sequence: 2 givenname: Shuhui surname: Chu fullname: Chu, Shuhui organization: Department of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California, 92697, United States of America – sequence: 3 givenname: Aimee L surname: Pierce fullname: Pierce, Aimee L organization: UCI Institute for Memory Impairment and Neurological Disorders, University of California Irvine, Irvine, California, 92697, United States of America – sequence: 4 givenname: William D surname: Brubaker fullname: Brubaker, William D organization: SRI International, Menlo Park, California, 94025, United States of America – sequence: 5 givenname: Richard E surname: Hauhart fullname: Hauhart, Richard E organization: Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, 63110, United States of America – sequence: 6 givenname: Diego surname: Mastroeni fullname: Mastroeni, Diego organization: School for Mental Health and Neuroscience (MHeNS), Department of Psychiatry and Neuropsychology, Faculty of Health, Medicine and Life Sciences, European Graduate School of Neuroscience (EURON), Maastricht University Medical Centre, Maastricht, The Netherlands – sequence: 7 givenname: Elizabeth V surname: Clarke fullname: Clarke, Elizabeth V organization: Department of Molecular Biology and Biochemistry, University of California Irvine, Irvine, California, 92697, United States of America – sequence: 8 givenname: Joseph surname: Rogers fullname: Rogers, Joseph organization: SRI International, Menlo Park, California, 94025, United States of America – sequence: 9 givenname: John P surname: Atkinson fullname: Atkinson, John P organization: Division of Rheumatology, Department of Medicine, Washington University School of Medicine, St. Louis, Missouri, 63110, United States of America – sequence: 10 givenname: Andrea J surname: Tenner fullname: Tenner, Andrea J organization: Department of Neurobiology and Behavior and Department of Pathology and Laboratory Science, University of California Irvine, Irvine, California, 92697, United States of America |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26914463$$D View this record in MEDLINE/PubMed |
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Copyright | COPYRIGHT 2016 Public Library of Science 2016 Fonseca et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. 2016 Fonseca et al 2016 Fonseca et al |
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Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Current address: Department of Neurology, Oregon Health and Sciences University, Portland, Oregon, 97239, United States of America Competing Interests: The authors have declared that no competing interests exist. Current address: The Biodesign Institute, Neurodegenerative Disease Research Center (NDRC) Arizona State University, Tempe, Arizona, 85287, United States of America Conceived and designed the experiments: MIF SC WDB REH EVC JR JPA AJT. Performed the experiments: MIF SC WDB EVC DM REH. Analyzed the data: MIF SC WDB EVC REH JR JPA AJT. Contributed reagents/materials/analysis tools: ALP JPA JR. Wrote the paper: MIF SC JR DM JPA REH AJT. Patient evaluation: ALP. |
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Publisher_xml | – name: Public Library of Science – name: Public Library of Science (PLoS) |
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Snippet | Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer's disease (AD). Recent large genome wide... Chronic activation of the complement system and induced inflammation are associated with neuropathology in Alzheimer’s disease (AD). Recent large genome wide... |
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SubjectTerms | Aged Aged, 80 and over Alzheimer Disease - blood Alzheimer Disease - genetics Alzheimer Disease - metabolism Alzheimer's disease Alzheimers disease Analysis Antibodies Astrocytes Astrocytes - metabolism Binding Biochemistry Biology and Life Sciences Blood Blood cells Blood vessels Brain Brain - pathology Brain research Cell receptors Complement activation Complement C1q - metabolism Complement C3b - metabolism Complement component C1q Complement component C3b Development and progression Diagnosis Enzyme-linked immunosorbent assay Epitopes Erythrocytes Erythrocytes - metabolism Female Gene Expression Regulation Genetic aspects Genetic Predisposition to Disease - genetics Genomes Genotypes Humans Immune system Male Medicine Medicine and Health Sciences Molecular biology Neurodegenerative diseases Neurological disorders Neurosciences Parenchyma Physical Sciences Physiological aspects Plasma levels Polymorphism, Single Nucleotide Protein Transport Proteins Receptors, Complement 3b - blood Receptors, Complement 3b - genetics Receptors, Complement 3b - metabolism Red blood cells Research and Analysis Methods Rheumatology Single nucleotide polymorphisms Single-nucleotide polymorphism Staining Statistical analysis Statistical methods |
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Title | Analysis of the Putative Role of CR1 in Alzheimer's Disease: Genetic Association, Expression and Function |
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