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Updated: Dec 28, 2025

A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration

A Mouse Model of Orthopedic Surgery to Study Postoperative Cognitive Dysfunction and Tissue Regeneration

Published on: February 27, 2018

Muscle Injury Induces Postoperative Cognitive Dysfunction.

Lorna Guéniot^1,2,3, Victoria Lepere^1,4,5, Gabriela Ferreira De Medeiros¹

¹Institut Pasteur, Experimental Neuropathology Unit, Paris, France.

Scientific Reports

|February 19, 2020

Summary

This summary is machine-generated.

Muscle injury impacts brain function, causing memory deficits and neuroinflammation. This study introduces a novel mouse model to investigate the link between muscle damage and postoperative cognitive dysfunction (POCD).

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Area of Science:

Neuroscience
Surgical Complications
Muscle Injury Research

Background:

Postoperative cognitive dysfunction (POCD) is a significant complication following surgery, with unclear underlying mechanisms.
Existing rodent models for POCD have limitations in assessing behavioral impacts, especially concerning skeletal muscle injury.
The role of muscle injury in the development of POCD remains largely unexplored.

Purpose of the Study:

To establish and validate a physical model of muscle injury in mice to study its impact on POCD.
To investigate the early and late effects of muscle injury on cognitive function and brain changes.
To explore the role of microglial activation and neurotrophic factors in muscle injury-induced POCD.

Main Methods:

Utilized a physical model of muscle injury in CX3CR1^GFP/+ mice, which allows for visualization of microglial cells.
Employed morphological, behavioral, and molecular approaches to assess cognitive function and brain alterations.
Analyzed short- and long-term memory, microglial reactivity in the hippocampus, and the balance of brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF).

Main Results:

Muscle regeneration following injury led to alterations in both short- and long-term memory.
Significant microglial reactivity was observed in the brain, including the hippocampus, 24 hours post-injury.
An altered balance of BDNF and NGF was detected 28 days after muscle injury.

Conclusions:

Muscle injury can induce both early and late-onset neurological and cognitive deficits.
The developed CX3CR1^GFP/+ mouse model is suitable for investigating microglial roles in neuroinflammation and synaptic plasticity relevant to POCD.
This research highlights a novel connection between skeletal muscle injury and the pathophysiology of POCD.