ApoE facilitates the microglial response to amyloid plaque pathology
One of the hallmarks of Alzheimer's disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ) peptide. Apolipoprotein E (ApoE) influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric...
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| Published in | The Journal of experimental medicine Vol. 215; no. 4; pp. 1047 - 1058 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
Rockefeller University Press
02.04.2018
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| Subjects | |
| Online Access | Get full text |
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| Abstract | One of the hallmarks of Alzheimer's disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ) peptide. Apolipoprotein E (ApoE) influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric Aβ in the brain. In addition to influencing Aβ metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1ΔE9 and APPPS1-21 transgenic mice. We report that
deficiency reduced fibrillar plaque deposition, consistent with previous studies. However, fibrillar plaques in
-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct Aβ morphotypes in
-deficient mice. We also observed a significant reduction in fibrillar plaque-associated microgliosis and activated microglial gene expression in
-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology. |
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| AbstractList | One of the hallmarks of Alzheimer’s disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ) peptide. Apolipoprotein E (ApoE) influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric Aβ in the brain. In addition to influencing Aβ metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1ΔE9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition, consistent with previous studies. However, fibrillar plaques in Apoe-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct Aβ morphotypes in Apoe-deficient mice. We also observed a significant reduction in fibrillar plaque–associated microgliosis and activated microglial gene expression in Apoe-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology. Increasing evidence suggests that apoE influences the innate immune response in neurodegeneration. Here, Ulrich et al. report that apoE influences amyloid plaque morphology and the microglial response to amyloid plaques, along with plaque-associated neuronal toxicity.One of the hallmarks of Alzheimer’s disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ) peptide. Apolipoprotein E (ApoE) influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric Aβ in the brain. In addition to influencing Aβ metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1ΔE9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition, consistent with previous studies. However, fibrillar plaques in Apoe-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct Aβ morphotypes in Apoe-deficient mice. We also observed a significant reduction in fibrillar plaque–associated microgliosis and activated microglial gene expression in Apoe-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology. One of the hallmarks of Alzheimer's disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ) peptide. Apolipoprotein E (ApoE) influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric Aβ in the brain. In addition to influencing Aβ metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1ΔE9 and APPPS1-21 transgenic mice. We report that deficiency reduced fibrillar plaque deposition, consistent with previous studies. However, fibrillar plaques in -deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct Aβ morphotypes in -deficient mice. We also observed a significant reduction in fibrillar plaque-associated microgliosis and activated microglial gene expression in -deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology. Increasing evidence suggests that apoE influences the innate immune response in neurodegeneration. Here, Ulrich et al. report that apoE influences amyloid plaque morphology and the microglial response to amyloid plaques, along with plaque-associated neuronal toxicity. One of the hallmarks of Alzheimer’s disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ) peptide. Apolipoprotein E (ApoE) influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric Aβ in the brain. In addition to influencing Aβ metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1ΔE9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition, consistent with previous studies. However, fibrillar plaques in Apoe -deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct Aβ morphotypes in Apoe -deficient mice. We also observed a significant reduction in fibrillar plaque–associated microgliosis and activated microglial gene expression in Apoe -deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology. One of the hallmarks of Alzheimers disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-beta (A beta) peptide. Apolipoprotein E (ApoE) influences the deposition of amyloid pathology through affecting the clearance and aggregation of monomeric A beta in the brain. In addition to influencing A beta metabolism, increasing evidence suggests that apoE influences microglial function in neurodegenerative diseases. Here, we characterize the impact that apoE has on amyloid pathology and the innate immune response in APPPS1 Delta E9 and APPPS1-21 transgenic mice. We report that Apoe deficiency reduced fibrillar plaque deposition, consistent with previous studies. However, fibrillar plaques in Apoe-deficient mice exhibited a striking reduction in plaque compaction. Hyperspectral fluorescent imaging using luminescent conjugated oligothiophenes identified distinct A beta morphotypes in Apoe-deficient mice. We also observed a significant reduction in fibrillar plaque-associated microgliosis and activated microglial gene expression in Apoe-deficient mice, along with significant increases in dystrophic neurites around fibrillar plaques. Our results suggest that apoE is critical in stimulating the innate immune response to amyloid pathology. |
| Author | Song, Wilbur M Nilsson, K Peter Anderson, Elise Jiang, Hong Nyström, Sofie Zhou, Yingyue Ulland, Tyler K Choi, Seulah Reinartz, Mariska Colonna, Marco Ulrich, Jason D Wang, Yaming Mahan, Thomas E Holtzman, David M Stewart, Floy R |
| AuthorAffiliation | 1 Department of Neurology, Washington University School of Medicine, St. Louis, MO 2 Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO 3 Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO 4 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 5 Department of Chemistry, IFM, Linköping University, Linköping, Sweden 6 Radboud University Nijmegen, Nijmegen, Netherlands 7 Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN |
| AuthorAffiliation_xml | – name: 6 Radboud University Nijmegen, Nijmegen, Netherlands – name: 7 Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN – name: 3 Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO – name: 1 Department of Neurology, Washington University School of Medicine, St. Louis, MO – name: 5 Department of Chemistry, IFM, Linköping University, Linköping, Sweden – name: 2 Knight Alzheimer's Disease Research Center, Washington University School of Medicine, St. Louis, MO – name: 4 Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO |
| Author_xml | – sequence: 1 givenname: Jason D surname: Ulrich fullname: Ulrich, Jason D organization: Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO – sequence: 2 givenname: Tyler K orcidid: 0000-0002-6507-4989 surname: Ulland fullname: Ulland, Tyler K organization: Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO – sequence: 3 givenname: Thomas E surname: Mahan fullname: Mahan, Thomas E organization: Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO – sequence: 4 givenname: Sofie orcidid: 0000-0002-4303-4783 surname: Nyström fullname: Nyström, Sofie organization: Department of Chemistry, IFM, Linköping University, Linköping, Sweden – sequence: 5 givenname: K Peter surname: Nilsson fullname: Nilsson, K Peter organization: Department of Chemistry, IFM, Linköping University, Linköping, Sweden – sequence: 6 givenname: Wilbur M orcidid: 0000-0002-6608-4628 surname: Song fullname: Song, Wilbur M organization: Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO – sequence: 7 givenname: Yingyue surname: Zhou fullname: Zhou, Yingyue organization: Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO – sequence: 8 givenname: Mariska orcidid: 0000-0001-7964-7963 surname: Reinartz fullname: Reinartz, Mariska organization: Radboud University Nijmegen, Nijmegen, Netherlands – sequence: 9 givenname: Seulah surname: Choi fullname: Choi, Seulah organization: Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO – sequence: 10 givenname: Hong surname: Jiang fullname: Jiang, Hong organization: Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO – sequence: 11 givenname: Floy R surname: Stewart fullname: Stewart, Floy R organization: Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO – sequence: 12 givenname: Elise surname: Anderson fullname: Anderson, Elise organization: Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO – sequence: 13 givenname: Yaming surname: Wang fullname: Wang, Yaming organization: Eli Lilly and Company, Lilly Corporate Center, Indianapolis, IN – sequence: 14 givenname: Marco orcidid: 0000-0001-5222-4987 surname: Colonna fullname: Colonna, Marco email: mcolonna@pathology.wustl.edu organization: Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO mcolonna@pathology.wustl.edu – sequence: 15 givenname: David M orcidid: 0000-0002-3400-0856 surname: Holtzman fullname: Holtzman, David M email: holtzman@neuro.wustl.edu organization: Hope Center for Neurological Disorders, Washington University School of Medicine, St. Louis, MO |
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| Copyright | 2018 Ulrich et al. Copyright Rockefeller University Press Apr 2, 2018 2018 Ulrich et al. 2018 |
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| Issue | 4 |
| Language | English |
| License | 2018 Ulrich et al. This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms/). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/). |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 J.D. Ulrich, T.K. Ulland, and T.E. Mahan contributed equally to this paper. |
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| Snippet | One of the hallmarks of Alzheimer's disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ)... One of the hallmarks of Alzheimer’s disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-β (Aβ)... Increasing evidence suggests that apoE influences the innate immune response in neurodegeneration. Here, Ulrich et al. report that apoE influences amyloid... One of the hallmarks of Alzheimers disease is the presence of extracellular diffuse and fibrillar plaques predominantly consisting of the amyloid-beta (A beta)... |
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| SubjectTerms | Apolipoprotein E Axons Brain Deposition Fluorescence Fluoroscopic imaging Gene expression Immune clearance Immune response Immune system Innate immunity Metabolism Mice Neurodegeneration Neurodegenerative diseases Neuroimaging Neurological diseases Neurotoxicity Pathology Reduction Rodents Senile plaques Toxicity Transgenic mice β-Amyloid |
| Title | ApoE facilitates the microglial response to amyloid plaque pathology |
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