For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
8
views
39
references
 Top references
cited by
14
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      125
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Preoperative Sleep Disturbance Exaggerates Surgery-Induced Neuroinflammation and Neuronal Damage in Aged Mice

      research-article

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Postoperative cognitive dysfunction (POCD) is defined as new cognitive impairment (memory impairment and impaired performance) after surgery, especially in aged patients. Sleep disturbance is a common phenomenon before surgery that has been increasingly thought to affect patient recovery. However, little is known about the functional impact of preoperative sleep disturbance on POCD. Here, we showed that tibial fracture surgery induced cognitive deficit and production of proinflammatory cytokines interleukin-6 (IL-6) and IL-1 β, along with microglia and astrocyte activation, neuronal damage, and blood-brain barrier (BBB) disruption. Preoperative sleep disturbance enhanced the surgery-induced neuroinflammation, neuronal damage, BBB disruption, and memory impairment 24 h after surgery. Taken together, these results demonstrated that preoperative sleep disturbance aggravated postoperative cognitive function in aged mice and the mechanism may be related to central nervous system (CNS) inflammation and neuronal damage.

          Related collections

          Most cited references39

          • Record: found
          • Abstract: found
          • Article: not found

          Sleep and the price of plasticity: from synaptic and cellular homeostasis to memory consolidation and integration.

          Giulio Tononi, Chiara Cirelli (2014)
          Sleep is universal, tightly regulated, and its loss impairs cognition. But why does the brain need to disconnect from the environment for hours every day? The synaptic homeostasis hypothesis (SHY) proposes that sleep is the price the brain pays for plasticity. During a waking episode, learning statistical regularities about the current environment requires strengthening connections throughout the brain. This increases cellular needs for energy and supplies, decreases signal-to-noise ratios, and saturates learning. During sleep, spontaneous activity renormalizes net synaptic strength and restores cellular homeostasis. Activity-dependent down-selection of synapses can also explain the benefits of sleep on memory acquisition, consolidation, and integration. This happens through the offline, comprehensive sampling of statistical regularities incorporated in neuronal circuits over a lifetime. This Perspective considers the rationale and evidence for SHY and points to open issues related to sleep and plasticity. Copyright © 2014 Elsevier Inc. All rights reserved.
          Article 0 comments Cited 694 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Predictors of cognitive dysfunction after major noncardiac surgery.

            Terri Monk, B Craig Weldon, Cyndi Garvan … (2008)
            The authors designed a prospective longitudinal study to investigate the hypothesis that advancing age is a risk factor for postoperative cognitive dysfunction (POCD) after major noncardiac surgery and the impact of POCD on mortality in the first year after surgery. One thousand sixty-four patients aged 18 yr or older completed neuropsychological tests before surgery, at hospital discharge, and 3 months after surgery. Patients were categorized as young (18-39 yr), middle-aged (40-59 yr), or elderly (60 yr or older). At 1 yr after surgery, patients were contacted to determine their survival status. At hospital discharge, POCD was present in 117 (36.6%) young, 112 (30.4%) middle-aged, and 138 (41.4%) elderly patients. There was a significant difference between all age groups and the age-matched control subjects (P < 0.001). At 3 months after surgery, POCD was present in 16 (5.7%) young, 19 (5.6%) middle-aged, and 39 (12.7%) elderly patients. At this time point, the prevalence of cognitive dysfunction was similar between age-matched controls and young and middle-aged patients but significantly higher in elderly patients compared to elderly control subjects (P < 0.001). The independent risk factors for POCD at 3 months after surgery were increasing age, lower educational level, a history of previous cerebral vascular accident with no residual impairment, and POCD at hospital discharge. Patients with POCD at hospital discharge were more likely to die in the first 3 months after surgery (P = 0.02). Likewise, patients who had POCD at both hospital discharge and 3 months after surgery were more likely to die in the first year after surgery (P = 0.02). Cognitive dysfunction is common in adult patients of all ages at hospital discharge after major noncardiac surgery, but only the elderly (aged 60 yr or older) are at significant risk for long-term cognitive problems. Patients with POCD are at an increased risk of death in the first year after surgery.
            Article 0 comments Cited 388 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Resolving postoperative neuroinflammation and cognitive decline.

              Niccolò Terrando, Lars Eriksson, Jae Ryu … (2011)
              Cognitive decline accompanies acute illness and surgery, especially in the elderly. Surgery engages the innate immune system that launches a systemic inflammatory response that, if unchecked, can cause multiple organ dysfunction. We sought to understand the mechanisms whereby the brain is targeted by the inflammatory response and how this can be resolved. C57BL/6J, Ccr2(RFP/+)Cx3cr1(GFP/+), Ikk(F/F) mice and LysM-Cre/Ikk(F/F) mice underwent stabilized tibial fracture operation under analgesia and general anesthesia. Separate cohorts of mice were tested for systemic and hippocampal inflammation, integrity of the blood-brain barrier (BBB), and cognition. The putative resolving effects of the cholinergic pathway on these postoperative responses were also studied. Peripheral surgery disrupts the BBB via release of tumor necrosis factor-alpha (TNFα), which facilitates the migration of macrophages into the hippocampus. Macrophage-specific deletion of Ikappa B kinase (IKK)β, a central coordinator of TNFα signaling through activation of nuclear factor (NF) κB, prevents BBB disruption and macrophage infiltration in the hippocampus following surgery. Activation of the α7 subtype of nicotinic acetylcholine receptors, an endogenous inflammation-resolving pathway, prevents TNFα-induced NF-κB activation, macrophage migration into the hippocampus, and cognitive decline following surgery. These data reveal the mechanisms for bidirectional communication between the brain and immune system following aseptic trauma. Pivotal molecular mechanisms can be targeted to prevent and/or resolve postoperative neuroinflammation and cognitive decline. Copyright © 2011 American Neurological Association.
              Article 0 comments Cited 214 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Contributors
                Yanning Qian:
                ORCID: http://orcid.org/0000-0002-7921-1681
                Jie Sun:
                ORCID: http://orcid.org/0000-0002-7456-9326
                Journal
                Journal ID (nlm-ta): Mediators Inflamm
                Journal ID (iso-abbrev): Mediators Inflamm
                Journal ID (publisher-id): MI
                Title: Mediators of Inflammation
                Publisher: Hindawi
                ISSN (Print): 0962-9351
                ISSN (Electronic): 1466-1861
                Publication date Collection: 2019
                Publication date (Electronic): 18 March 2019
                Volume: 2019
                Electronic Location Identifier: 8301725
                Affiliations
                Department of Anesthesiology, The First Affiliated Hospital of Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu 210029, China
                Author notes

                Academic Editor: Daniela Caccamo

                Author information
                http://orcid.org/0000-0002-7921-1681
                http://orcid.org/0000-0002-7456-9326
                Article
                DOI: 10.1155/2019/8301725
                PMC ID: 6442479
                PubMed ID: 31011286
                SO-VID: 6fd5af7e-10dc-4a3e-a34b-74e05230386d
                Copyright © Copyright © 2019 Pengfei Ni et al.
                License:

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                Date received : 18 September 2018
                Date accepted : 23 December 2018
                Funding
                Funded by: Priority Academic Program Development of Jiangsu Higher Education Institutions
                Funded by: Natural Science Foundation of Jiangsu Province
                Award ID: BK20171088
                Funded by: National Natural Science Foundation of China
                Award ID: 81701375
                Award ID: 81671387
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Immunology
                Data availability:
                ScienceOpen disciplines: Immunology

                Comments

                Comment on this article

                scite_

                Similar content125

                See all similar

                Cited by14

                See all cited by

                Most referenced authors709

                See all reference authors