Muscle Injury Induces Postoperative Cognitive Dysfunction

Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to months after hospital discharge, and its pathophysiology still remains unclear. Translational research focusing on POCD is based on a wide va...

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Vydáno v:Scientific reports Ročník 10; číslo 1; s. 2768
Hlavní autoři: Guéniot, Lorna, Lepere, Victoria, De Medeiros, Gabriela Ferreira, Danckaert, Anne, Flamant, Patricia, Le Dudal, Marine, Langeron, Olivier, Goossens, Pierre L., Chrétien, Fabrice, Jouvion, Grégory
Médium: Journal Article
Jazyk:angličtina
Vydáno: London Nature Publishing Group UK 17.02.2020
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ISSN:2045-2322, 2045-2322
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Abstract Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to months after hospital discharge, and its pathophysiology still remains unclear. Translational research focusing on POCD is based on a wide variety of rodent models, such as the murine tibial fracture, whose severity can limit mouse locomotion and proper behavioral assessment. Besides, influence of skeletal muscle injury, a lesion encountered in a wide range of surgeries, has not been explored in POCD occurrence. We propose a physical model of muscle injury in CX3CR1 GFP/+ mice (displaying green fluorescent microglial cells) to study POCD, with morphological, behavioral and molecular approaches. We highlighted: alteration of short- and long-term memory after muscle regeneration, wide microglial reactivity in the brain, including hippocampus area, 24 hours after muscle injury, and an alteration of central brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) balance, 28 days after muscle injury. Our results suggest for the first time that muscle injury can have early as well as late impacts on the brain. Our CX3CR1 GFP/+ model can also facilitate microglial investigation, more specifically their pivotal role in neuroinflammation and synaptic plasticity, in the pathophysiology of POCD.
AbstractList Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to months after hospital discharge, and its pathophysiology still remains unclear. Translational research focusing on POCD is based on a wide variety of rodent models, such as the murine tibial fracture, whose severity can limit mouse locomotion and proper behavioral assessment. Besides, influence of skeletal muscle injury, a lesion encountered in a wide range of surgeries, has not been explored in POCD occurrence. We propose a physical model of muscle injury in CX3CR1 GFP/+ mice (displaying green fluorescent microglial cells) to study POCD, with morphological, behavioral and molecular approaches. We highlighted: alteration of short- and long-term memory after muscle regeneration, wide microglial reactivity in the brain, including hippocampus area, 24 hours after muscle injury, and an alteration of central brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) balance, 28 days after muscle injury. Our results suggest for the first time that muscle injury can have early as well as late impacts on the brain. Our CX3CR1 GFP/+ model can also facilitate microglial investigation, more specifically their pivotal role in neuroinflammation and synaptic plasticity, in the pathophysiology of POCD.
Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to months after hospital discharge, and its pathophysiology still remains unclear. Translational research focusing on POCD is based on a wide variety of rodent models, such as the murine tibial fracture, whose severity can limit mouse locomotion and proper behavioral assessment. Besides, influence of skeletal muscle injury, a lesion encountered in a wide range of surgeries, has not been explored in POCD occurrence. We propose a physical model of muscle injury in CX3CR1GFP/+ mice (displaying green fluorescent microglial cells) to study POCD, with morphological, behavioral and molecular approaches. We highlighted: alteration of short- and long-term memory after muscle regeneration, wide microglial reactivity in the brain, including hippocampus area, 24 hours after muscle injury, and an alteration of central brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) balance, 28 days after muscle injury. Our results suggest for the first time that muscle injury can have early as well as late impacts on the brain. Our CX3CR1GFP/+ model can also facilitate microglial investigation, more specifically their pivotal role in neuroinflammation and synaptic plasticity, in the pathophysiology of POCD.
Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to months after hospital discharge, and its pathophysiology still remains unclear. Translational research focusing on POCD is based on a wide variety of rodent models, such as the murine tibial fracture, whose severity can limit mouse locomotion and proper behavioral assessment. Besides, influence of skeletal muscle injury, a lesion encountered in a wide range of surgeries, has not been explored in POCD occurrence. We propose a physical model of muscle injury in CX3CR1 mice (displaying green fluorescent microglial cells) to study POCD, with morphological, behavioral and molecular approaches. We highlighted: alteration of short- and long-term memory after muscle regeneration, wide microglial reactivity in the brain, including hippocampus area, 24 hours after muscle injury, and an alteration of central brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) balance, 28 days after muscle injury. Our results suggest for the first time that muscle injury can have early as well as late impacts on the brain. Our CX3CR1 model can also facilitate microglial investigation, more specifically their pivotal role in neuroinflammation and synaptic plasticity, in the pathophysiology of POCD.
Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to months after hospital discharge, and its pathophysiology still remains unclear. Translational research focusing on POCD is based on a wide variety of rodent models, such as the murine tibial fracture, whose severity can limit mouse locomotion and proper behavioral assessment. Besides, influence of skeletal muscle injury, a lesion encountered in a wide range of surgeries, has not been explored in POCD occurrence. We propose a physical model of muscle injury in CX3CR1GFP/+ mice (displaying green fluorescent microglial cells) to study POCD, with morphological, behavioral and molecular approaches. We highlighted: alteration of short- and long-term memory after muscle regeneration, wide microglial reactivity in the brain, including hippocampus area, 24 hours after muscle injury, and an alteration of central brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) balance, 28 days after muscle injury. Our results suggest for the first time that muscle injury can have early as well as late impacts on the brain. Our CX3CR1GFP/+ model can also facilitate microglial investigation, more specifically their pivotal role in neuroinflammation and synaptic plasticity, in the pathophysiology of POCD.Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to months after hospital discharge, and its pathophysiology still remains unclear. Translational research focusing on POCD is based on a wide variety of rodent models, such as the murine tibial fracture, whose severity can limit mouse locomotion and proper behavioral assessment. Besides, influence of skeletal muscle injury, a lesion encountered in a wide range of surgeries, has not been explored in POCD occurrence. We propose a physical model of muscle injury in CX3CR1GFP/+ mice (displaying green fluorescent microglial cells) to study POCD, with morphological, behavioral and molecular approaches. We highlighted: alteration of short- and long-term memory after muscle regeneration, wide microglial reactivity in the brain, including hippocampus area, 24 hours after muscle injury, and an alteration of central brain derived neurotrophic factor (BDNF) and nerve growth factor (NGF) balance, 28 days after muscle injury. Our results suggest for the first time that muscle injury can have early as well as late impacts on the brain. Our CX3CR1GFP/+ model can also facilitate microglial investigation, more specifically their pivotal role in neuroinflammation and synaptic plasticity, in the pathophysiology of POCD.
ArticleNumber 2768
Author Flamant, Patricia
Lepere, Victoria
Jouvion, Grégory
Langeron, Olivier
Le Dudal, Marine
De Medeiros, Gabriela Ferreira
Chrétien, Fabrice
Goossens, Pierre L.
Danckaert, Anne
Guéniot, Lorna
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  organization: Institut Pasteur, Experimental Neuropathology Unit, Multidisciplinary Intensive Care Unit, Department of Anesthesiology and Critical Care, La Pitié-Salpêtrière Hospital, Assistance Publique-Hôpitaux de Paris, Sorbonne Université, Polyvalent Surgical Resuscitation, La Pitié-Salpêtrière Hospital, Assistance Publique-Hôpitaux de Paris, Sorbonne University
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  givenname: Gabriela Ferreira
  surname: De Medeiros
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  fullname: Langeron, Olivier
  organization: Institut Pasteur, Experimental Neuropathology Unit, Department of Anesthesia and Critical Care, Hôpitaux Universitaires Henri Mondor-Créteil-Assistance Publique Hôpitaux de Paris, Paris-Est Créteil University
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  fullname: Chrétien, Fabrice
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  givenname: Grégory
  orcidid: 0000-0003-0188-2554
  surname: Jouvion
  fullname: Jouvion, Grégory
  email: gregory.jouvion@pasteur.fr
  organization: Institut Pasteur, Experimental Neuropathology Unit, Sorbonne Université, INSERM, Pathophysiology of pediatric genetic diseases, Assistance Publique-Hôpitaux de Paris, Hôpital Armand-Trousseau, UF Génétique moléculaire
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Snippet Postoperative cognitive dysfunction (POCD) is a major complication affecting patients of any age undergoing surgery. This syndrome impacts everyday life up to...
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StartPage 2768
SubjectTerms 14/19
631/378/371
64/110
692/617/375
96/63
Aging - pathology
Animal cognition
Animal models
Animals
Behavioral plasticity
Brain - pathology
Brain - surgery
Brain research
Brain-derived neurotrophic factor
Brain-Derived Neurotrophic Factor - metabolism
Cognitive ability
Cognitive science
Critical care
CX3C Chemokine Receptor 1 - genetics
Cytokines - metabolism
Disease Models, Animal
Experiments
Hippocampus - injuries
Hippocampus - pathology
Hippocampus - surgery
Human health and pathology
Humanities and Social Sciences
Humans
Inflammation
Life Sciences
Locomotion
Long term memory
Male
Memory
Mice
Microglia
Microglia - pathology
Morphology
multidisciplinary
Muscle, Skeletal - injuries
Muscle, Skeletal - metabolism
Muscle, Skeletal - pathology
Muscle, Skeletal - surgery
Nerve growth factor
Nerve Growth Factor - metabolism
Pathophysiology
Postoperative Cognitive Complications - etiology
Postoperative Cognitive Complications - metabolism
Postoperative Cognitive Complications - pathology
Postoperative Complications - etiology
Postoperative Complications - metabolism
Postoperative Complications - pathology
Regeneration
Science
Science (multidisciplinary)
Skeletal muscle
Surgery
Synaptic plasticity
Young adults
Title Muscle Injury Induces Postoperative Cognitive Dysfunction
URI https://link.springer.com/article/10.1038/s41598-020-59639-3
https://www.ncbi.nlm.nih.gov/pubmed/32066806
https://www.proquest.com/docview/2356657903
https://www.proquest.com/docview/2357460064
https://inserm.hal.science/inserm-02503658
https://pubmed.ncbi.nlm.nih.gov/PMC7026159
Volume 10
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