Abstract

Postoperative cognitive dysfunction (POCD), as one of the common postoperative complications, mainly occurs after surgery and anesthesia, especially in the elderly. It refers to cognitive function changes such as decreased learning and memory ability and inability to concentrate. In severe cases, there could be personality changes and a decline in social behavior. At present, a great deal of research had been carried out on POCD, but its specific mechanism remains unclear. The release of peripheral inflammation-related factors, the degradation and destruction of the blood-brain barrier, the occurrence of central inflammation, and the neuronal apoptosis and synaptic loss could be promoted by neuroinflammation indicating that inflammatory mechanisms may play key roles in the occurrence of POCD.

Highlights

  • With the development of modern medicine, a growing number of elderly patients have the possibility to receive one or more life-extending surgical procedures [1]

  • It was detrimental to brain function. These previous studies had shown that COX-2 was involved in synaptic transmission and plasticity while Prostaglandin E2 (PGE2), a key molecule in COX-2-mediated synaptic modification, played an indispensable role

  • Inflammatory cytokines produced by surgical or anesthetic factors crossed the blood-brain barrier (BBB) and entered to the central nervous system (CNS) to cause the central inflammatory cell activation. These inflammatory cells would continue to release a series of pathological proteins such as inflammatory cytokines, injurious proteins, and neurotoxins, which could interact with neurons and synapses, resulting in neuronal death, synaptic loss, and the inability of cell signaling, eventually leading to the occurrence of postoperative cognitive dysfunction (POCD) [124]

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Summary

Introduction

With the development of modern medicine, a growing number of elderly patients have the possibility to receive one or more life-extending surgical procedures [1]. Postoperative cognitive dysfunction (POCD), as one of the common complications after surgery, had seriously threatened the quality of life especially for the elderly patients, extended the length of hospital stay, and increased the medical cost [2]. Postoperative cognitive dysfunction had been broadly defined as a significant decrease in cognitive ability following surgery or anesthesia [6]. Many researchers had successfully established POCD models by intraperitoneal injection of lipopolysaccharide (LPS) to mice to induce neuroinflammation, and more attention had been paid to the mechanism of neuroinflammation caused by surgery or anesthesia in POCD animals [6, 9]. This review will discuss the research progress of POCD from the perspective of inflammatory mechanisms

POCD and Inflammation-Related Factors
POCD and the Blood-Brain Barrier
POCD and the Gut-Brain Axis
POCD and Microglia
POCD and Neurons and Synapses
Possible Prevention and Therapeutic Ways
Conclusions
Findings
Conflicts of Interest
Full Text
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