Inhibition of IL-12/IL-23 signaling reduces Alzheimer's disease–like pathology and cognitive decline
Proinflammatory cytokine expression increases as a result of amyloid deposition in Alzheimer's disease. Frank L. Heppner and colleagues show that genetic and pharmacological inhibition of IL-12 and IL-23 signaling reduces plaque load and improves cognitive deficits in mouse models of Alzheimer&...
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| Published in | Nature medicine Vol. 18; no. 12; pp. 1812 - 1819 |
|---|---|
| Main Authors | , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
New York
Nature Publishing Group US
01.12.2012
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1078-8956 1546-170X 1546-170X |
| DOI | 10.1038/nm.2965 |
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| Abstract | Proinflammatory cytokine expression increases as a result of amyloid deposition in Alzheimer's disease. Frank L. Heppner and colleagues show that genetic and pharmacological inhibition of IL-12 and IL-23 signaling reduces plaque load and improves cognitive deficits in mouse models of Alzheimer's disease. As the concentration of p40 is also increased in the cerebrospinal fluid of individuals with Alzheimer's disease, this suggests that this pathway may be targeted therapeutically in patients.
The pathology of Alzheimer's disease has an inflammatory component that is characterized by upregulation of proinflammatory cytokines, particularly in response to amyloid-β (Aβ). Using the
APPPS1
Alzheimer's disease mouse model, we found increased production of the common interleukin-12 (IL-12) and IL-23 subunit p40 by microglia. Genetic ablation of the IL-12/IL-23 signaling molecules p40, p35 or p19, in which deficiency of p40 or its receptor complex had the strongest effect, resulted in decreased cerebral amyloid load. Although deletion of IL-12/IL-23 signaling from the radiation-resistant glial compartment of the brain was most efficient in mitigating cerebral amyloidosis, peripheral administration of a neutralizing p40-specific antibody likewise resulted in a reduction of cerebral amyloid load in
APPPS1
mice. Furthermore, intracerebroventricular delivery of antibodies to p40 significantly reduced the concentration of soluble Aβ species and reversed cognitive deficits in aged
APPPS1
mice. The concentration of p40 was also increased in the cerebrospinal fluid of subjects with Alzheimer's disease, which suggests that inhibition of the IL-12/IL-23 pathway may attenuate Alzheimer's disease pathology and cognitive deficits. |
|---|---|
| AbstractList | The pathology of Alzheimer's disease has an inflammatory component that is characterized by upregulation of proinflammatory cytokines, particularly in response to amyloid- beta (A beta ). Using the APPPS1 Alzheimer's disease mouse model, we found increased production of the common interleukin-12 (IL-12) and IL-23 subunit p40 by microglia. Genetic ablation of the IL-12/IL-23 signaling molecules p40, p35 or p19, in which deficiency of p40 or its receptor complex had the strongest effect, resulted in decreased cerebral amyloid load. Although deletion of IL-12/IL-23 signaling from the radiation-resistant glial compartment of the brain was most efficient in mitigating cerebral amyloidosis, peripheral administration of a neutralizing p40-specific antibody likewise resulted in a reduction of cerebral amyloid load in APPPS1 mice. Furthermore, intracerebroventricular delivery of antibodies to p40 significantly reduced the concentration of soluble A beta species and reversed cognitive deficits in aged APPPS1 mice. The concentration of p40 was also increased in the cerebrospinal fluid of subjects with Alzheimer's disease, which suggests that inhibition of the IL-12/IL-23 pathway may attenuate Alzheimer's disease pathology and cognitive deficits. The pathology of Alzheimer's disease has an inflammatory component that is characterized by upregulation of proinflammatory cytokines, particularly in response to amyloid-β (Aβ). Using the APPPS1 Alzheimer's disease mouse model, we found increased production of the common interleukin-12 (IL-12) and IL-23 subunit p40 by microglia. Genetic ablation of the IL-12/IL-23 signaling molecules p40, p35 or p19, in which deficiency of p40 or its receptor complex had the strongest effect, resulted in decreased cerebral amyloid load. Although deletion of IL-12/IL-23 signaling from the radiation-resistant glial compartment of the brain was most efficient in mitigating cerebral amyloidosis, peripheral administration of a neutralizing p40-specific antibody likewise resulted in a reduction of cerebral amyloid load in APPPS1 mice. Furthermore, intracerebroventricular delivery of antibodies to p40 significantly reduced the concentration of soluble Aβ species and reversed cognitive deficits in aged APPPS1 mice. The concentration of p40 was also increased in the cerebrospinal fluid of subjects with Alzheimer's disease, which suggests that inhibition of the IL-12/IL-23 pathway may attenuate Alzheimer's disease pathology and cognitive deficits. The pathology of Alzheimer's disease has an inflammatory component that is characterized by upregulation of proinflammatory cytokines, particularly in response to amyloid-β (A13). Using the APPPS1 Alzheimer's disease mouse model, we found increased production of the common interleukin-12 (IL-12) and IL-23 subunit p40 by microglia. Genetic ablation of the IL-12/IL-23 signaling molecules p40, p35 or p19, in which deficiency of p40 or its receptor complex had the strongest effect, resulted in decreased cerebral amyloid load. Although deletion of IL-12/IL-23 signaling from the radiation-resistant glial compartment of the brain was most efficient in mitigating cerebral amyloidosis, peripheral administration of a neutralizing p40-specific antibody likewise resulted in a reduction of cerebral amyloid load in APPPS1 mice. Furthermore, intracerebroventricular delivery of antibodies to p40 significantly reduced the concentration of soluble A13 species and reversed cognitive deficits in aged APPPS1 mice. The concentration of p40 was also increased in the cerebrospinal fluid of subjects with Alzheimer's disease, which suggests that inhibition of the IL-12/IL-23 pathway may attenuate Alzheimer's disease pathology and cognitive deficits. Proinflammatory cytokine expression increases as a result of amyloid deposition in Alzheimer's disease. Frank L. Heppner and colleagues show that genetic and pharmacological inhibition of IL-12 and IL-23 signaling reduces plaque load and improves cognitive deficits in mouse models of Alzheimer's disease. As the concentration of p40 is also increased in the cerebrospinal fluid of individuals with Alzheimer's disease, this suggests that this pathway may be targeted therapeutically in patients. The pathology of Alzheimer's disease has an inflammatory component that is characterized by upregulation of proinflammatory cytokines, particularly in response to amyloid-β (Aβ). Using the APPPS1 Alzheimer's disease mouse model, we found increased production of the common interleukin-12 (IL-12) and IL-23 subunit p40 by microglia. Genetic ablation of the IL-12/IL-23 signaling molecules p40, p35 or p19, in which deficiency of p40 or its receptor complex had the strongest effect, resulted in decreased cerebral amyloid load. Although deletion of IL-12/IL-23 signaling from the radiation-resistant glial compartment of the brain was most efficient in mitigating cerebral amyloidosis, peripheral administration of a neutralizing p40-specific antibody likewise resulted in a reduction of cerebral amyloid load in APPPS1 mice. Furthermore, intracerebroventricular delivery of antibodies to p40 significantly reduced the concentration of soluble Aβ species and reversed cognitive deficits in aged APPPS1 mice. The concentration of p40 was also increased in the cerebrospinal fluid of subjects with Alzheimer's disease, which suggests that inhibition of the IL-12/IL-23 pathway may attenuate Alzheimer's disease pathology and cognitive deficits. The pathology of Alzheimer's disease has an inflammatory component that is characterized by upregulation of proinflammatory cytokines, particularly in response to amyloid-β (Aβ). Using the APPPS1 Alzheimer's disease mouse model, we found increased production of the common interleukin-12 (IL-12) and IL-23 subunit p40 by microglia. Genetic ablation of the IL-12/IL-23 signaling molecules p40, p35 or p19, in which deficiency of p40 or its receptor complex had the strongest effect, resulted in decreased cerebral amyloid load. Although deletion of IL-12/IL-23 signaling from the radiation-resistant glial compartment of the brain was most efficient in mitigating cerebral amyloidosis, peripheral administration of a neutralizing p40-specific antibody likewise resulted in a reduction of cerebral amyloid load in APPPS1 mice. Furthermore, intracerebroventricular delivery of antibodies to p40 significantly reduced the concentration of soluble Aβ species and reversed cognitive deficits in aged APPPS1 mice. The concentration of p40 was also increased in the cerebrospinal fluid of subjects with Alzheimer's disease, which suggests that inhibition of the IL-12/IL-23 pathway may attenuate Alzheimer's disease pathology and cognitive deficits.The pathology of Alzheimer's disease has an inflammatory component that is characterized by upregulation of proinflammatory cytokines, particularly in response to amyloid-β (Aβ). Using the APPPS1 Alzheimer's disease mouse model, we found increased production of the common interleukin-12 (IL-12) and IL-23 subunit p40 by microglia. Genetic ablation of the IL-12/IL-23 signaling molecules p40, p35 or p19, in which deficiency of p40 or its receptor complex had the strongest effect, resulted in decreased cerebral amyloid load. Although deletion of IL-12/IL-23 signaling from the radiation-resistant glial compartment of the brain was most efficient in mitigating cerebral amyloidosis, peripheral administration of a neutralizing p40-specific antibody likewise resulted in a reduction of cerebral amyloid load in APPPS1 mice. Furthermore, intracerebroventricular delivery of antibodies to p40 significantly reduced the concentration of soluble Aβ species and reversed cognitive deficits in aged APPPS1 mice. The concentration of p40 was also increased in the cerebrospinal fluid of subjects with Alzheimer's disease, which suggests that inhibition of the IL-12/IL-23 pathway may attenuate Alzheimer's disease pathology and cognitive deficits. |
| Audience | Academic |
| Author | vom Berg, Johannes Mair, Florian Becher, Burkhard Heppner, Frank L Peters, Oliver Miller, Kelly R Winter, York Kälin, Roland E Schipke, Carola G Wegner, Anja Obst, Juliane Lopategui-Cabezas, Ileana Prokop, Stefan |
| Author_xml | – sequence: 1 givenname: Johannes surname: vom Berg fullname: vom Berg, Johannes organization: Institute of Experimental Immunology, University of Zürich – sequence: 2 givenname: Stefan surname: Prokop fullname: Prokop, Stefan organization: Department of Neuropathology, Charité–Universitätsmedizin Berlin – sequence: 3 givenname: Kelly R surname: Miller fullname: Miller, Kelly R organization: Department of Neuropathology, Charité–Universitätsmedizin Berlin – sequence: 4 givenname: Juliane surname: Obst fullname: Obst, Juliane organization: Department of Neuropathology, Charité–Universitätsmedizin Berlin – sequence: 5 givenname: Roland E surname: Kälin fullname: Kälin, Roland E organization: Department of Neuropathology, Charité–Universitätsmedizin Berlin – sequence: 6 givenname: Ileana surname: Lopategui-Cabezas fullname: Lopategui-Cabezas, Ileana organization: Department of Neuropathology, Charité–Universitätsmedizin Berlin, Present address: Institute of Basic and Preclinical Sciences 'Victoria de Girón', Medical University of Havana, Havana, Cuba – sequence: 7 givenname: Anja surname: Wegner fullname: Wegner, Anja organization: Department of Neuropathology, Charité–Universitätsmedizin Berlin – sequence: 8 givenname: Florian surname: Mair fullname: Mair, Florian organization: Institute of Experimental Immunology, University of Zürich – sequence: 9 givenname: Carola G surname: Schipke fullname: Schipke, Carola G organization: Department of Neuropathology, Charité–Universitätsmedizin Berlin, Department of Psychiatry, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin – sequence: 10 givenname: Oliver surname: Peters fullname: Peters, Oliver organization: Department of Psychiatry, Charité–Universitätsmedizin Berlin, Campus Benjamin Franklin – sequence: 11 givenname: York surname: Winter fullname: Winter, York organization: Cognitive Neurobiology and Berlin Mouse Clinic for Neurology and Psychiatry, Humboldt University – sequence: 12 givenname: Burkhard surname: Becher fullname: Becher, Burkhard email: becher@immunology.uzh.ch organization: Institute of Experimental Immunology, University of Zürich – sequence: 13 givenname: Frank L surname: Heppner fullname: Heppner, Frank L email: frank.heppner@charite.de organization: Department of Neuropathology, Charité–Universitätsmedizin Berlin |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/23178247$$D View this record in MEDLINE/PubMed |
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| Snippet | Proinflammatory cytokine expression increases as a result of amyloid deposition in Alzheimer's disease. Frank L. Heppner and colleagues show that genetic and... The pathology of Alzheimer's disease has an inflammatory component that is characterized by upregulation of proinflammatory cytokines, particularly in response... |
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| SubjectTerms | 631/250/127/1213 631/250/516 692/699/375/365/1283 692/700/139/422 Alzheimer Disease - pathology Alzheimer's disease Amyloid beta-Peptides - metabolism Analysis of Variance Animals Antibodies - administration & dosage Antibodies - pharmacology Biomedicine Blotting, Western Cancer Research Care and treatment Cognition & reasoning Cognition - drug effects Cognitive ability Complications and side effects Disease DNA Primers - genetics Enzyme-Linked Immunosorbent Assay Flow Cytometry Genetic aspects Health aspects Infectious Diseases Injections, Intraperitoneal Interleukin-12 - genetics Interleukin-12 - immunology Interleukin-12 - metabolism Interleukin-12 Subunit p40 - cerebrospinal fluid Interleukin-12 Subunit p40 - genetics Interleukin-12 Subunit p40 - immunology Interleukin-12 Subunit p40 - metabolism Interleukins Memory, Disorders of Metabolic Diseases Mice Mice, Transgenic Microglia - metabolism Molecular Medicine Neurosciences Pathology Real-Time Polymerase Chain Reaction Risk factors Signal Transduction - drug effects Signaling Statistics |
| Title | Inhibition of IL-12/IL-23 signaling reduces Alzheimer's disease–like pathology and cognitive decline |
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