AI Article Synopsis

  • Postoperative cognitive dysfunction (POCD) affects patients of all ages after surgery, leading to long-lasting cognitive issues and an unclear underlying cause.
  • Research using rodent models, particularly muscle injury models, is proposed to study the link between POCD and skeletal muscle damage.
  • Findings indicate that muscle injury leads to both short- and long-term memory alterations, significant microglial activity in the brain, and changes in neurotrophic factors, suggesting early and late brain impacts from muscle injury connected to POCD.

Article 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 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.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7026159PMC
http://dx.doi.org/10.1038/s41598-020-59639-3DOI Listing

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