Tumor necrosis factor-[alpha] triggers a cytokine cascade yielding postoperative cognitive decline
Cognitive decline following surgery in older individuals is a major clinical problem of uncertain mechanism; a similar cognitive decline also follows severe infection, chemotherapy, or trauma and is currently without effective therapy. A variety of mechanisms have been proposed, and exploring the ro...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2010-11, Vol.107 (47), p.20518-20522 |
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| container_issue | 47 |
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| container_title | Proceedings of the National Academy of Sciences - PNAS |
| container_volume | 107 |
| creator | Terrando, Niccolò Monaco, Claudia Ma, Daqing Foxwell, Brian M J Feldmann, Marc Maze, Mervyn |
| description | Cognitive decline following surgery in older individuals is a major clinical problem of uncertain mechanism; a similar cognitive decline also follows severe infection, chemotherapy, or trauma and is currently without effective therapy. A variety of mechanisms have been proposed, and exploring the role of inflammation, we recently reported the role of IL-1β in the hippocampus after surgery in mice with postoperative cognitive dysfunction. Here, we show that TNF-α is upstream of IL-1 and provokes its production in the brain. Peripheral blockade of TNF-α is able to limit the release of IL-1 and prevent neuroinflammation and cognitive decline in a mouse model of surgery-induced cognitive decline. TNF-α appears to synergize with MyD88, the IL-1/TLR superfamily common signaling pathway, to sustain postoperative cognitive decline. Taken together, our results suggest a unique therapeutic potential for preemptive treatment with anti-TNF antibody to prevent surgery-induced cognitive decline. [PUBLICATION ABSTRACT] |
| doi_str_mv | 10.1073/pnas.1014557107 |
| format | Article |
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A variety of mechanisms have been proposed, and exploring the role of inflammation, we recently reported the role of IL-1β in the hippocampus after surgery in mice with postoperative cognitive dysfunction. Here, we show that TNF-α is upstream of IL-1 and provokes its production in the brain. Peripheral blockade of TNF-α is able to limit the release of IL-1 and prevent neuroinflammation and cognitive decline in a mouse model of surgery-induced cognitive decline. TNF-α appears to synergize with MyD88, the IL-1/TLR superfamily common signaling pathway, to sustain postoperative cognitive decline. Taken together, our results suggest a unique therapeutic potential for preemptive treatment with anti-TNF antibody to prevent surgery-induced cognitive decline. 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| source | PubMed Central (PMC); Alma/SFX Local Collection; Free Full-Text Journals in Chemistry; JSTOR |
| subjects | Animal models Antibodies Brain Brain surgery Chemotherapy Cognition & reasoning Cognitive ability Cytokines Hippocampus Infection Inflammation Interleukin 1 MyD88 protein Proteins Rodents Signal transduction Surgery Synergism Trauma Tumor necrosis factor Tumor necrosis factor- alpha |
| title | Tumor necrosis factor-[alpha] triggers a cytokine cascade yielding postoperative cognitive decline |
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