Research progress on the association between MicroRNA and postoperative cognitive dysfunction.

Postoperative cognitive dysfunction (POCD) is a significant complication following surgery. The precise mechanisms underlying POCD remain elusive, although it is speculated that they involve central nervous system inflammation, oxidative stress and cellular apoptosis. MicroRNAs (miRNAs), a class of non-coding RNAs widely distributed in eukaryotes, have been implicated in the pathogenesis of neurodegenerative disorders and could potentially impact POCD. This review explores the association between miRNAs and POCD and provides an overview of the progress of current research on miRNAs in the pathogenesis, diagnosis, and treatment of POCD.

Current status of sevoflurane anesthesia in association with microglia inflammation and neurodegenerative diseases.

Sevoflurane is one of the most commonly used volatile anesthetics in clinical practice and is often used in pediatric anesthesia and intraoperative maintenance. Microglia exist in the central nervous system and are innate immune cells in the central nervous system. Under external stimulation, microglia are divided into two phenotypes: proinflammatory (M1 type) and anti-inflammatory (M2 type), maintaining the stability of the central nervous system through induction, housekeeping, and defense functions. Sevoflurane can activate microglia, increase the expression of inflammatory factors through various inflammatory signaling pathways, release inflammatory mediators to cause oxidative stress, damage nerve tissues, and eventually develop into neurodegenerative diseases. In this article, the relationship between sevoflurane anesthesia and microglia inflammation expression and the occurrence of neurodegenerative diseases is reviewed as follows.

Emerging Insights into Postoperative Neurocognitive Disorders: The Role of Signaling Across the Gut-Brain Axis.

The pathophysiological regulatory mechanisms in postoperative neurocognitive disorders (PNCDs) are intricately complex. Currently, the pathogenesis of PNCDs has not been fully elucidated. The mechanism involved may include a variety of factors, such as neuroinflammation, oxidative stress, and neuroendocrine dysregulation. Research into the gut microbiota-induced regulations on brain functions is increasingly becoming a focal point of exploration. Emerging evidence has shown that intestinal bacteria may play an essential role in maintaining the homeostasis of various physiological systems and regulating disease occurrence. Recent studies have confirmed the association of the gut-brain axis with central nervous system diseases. However, the regulatory effects of this axis in the pathogenesis of PNCDs remain unclear. Therefore, this paper intends to review the bidirectional signaling and mechanism of the gut-brain axis in PNCDs, summarize the latest research progress, and discuss the possible mechanism of intestinal bacteria affecting nervous system diseases. This review is aimed at providing a scientific reference for predicting the clinical risk of PNCD patients and identifying early diagnostic markers and prevention targets.

Research advances in the influence of lipid metabolism on cognitive impairment.

Cognitive impairment (CI) is a mental disorder related to cognition and understanding, which is mainly categorized into mild CI and senile dementia. This disease is associated with multiple factors, such as chronic brain injury, aging, chronic systemic disease, mental state, and psychological factors. However, the pathological mechanism of CI remains unclear; it is usually associated with such underlying diseases as diabetes and hyperlipidemia. It has been demonstrated that abundant lipid metabolism indexes in the human body are closely related to CI, including total cholesterol, high-density lipoprotein cholesterol, low-density lipoprotein cholesterol, triglycerides, apolipoprotein, and so forth. As a crucial risk factor for CI, hyperlipidemia is of great significance in the occurrence and development of CI. However, the specific correlation between dyslipidemia and CI is still not fully elucidated. Besides, the efficacy of lipid-lowering drugs in the prophylaxis and treatment of CI has not been clarified. In this study, relevant advances in the influence of lipid metabolism disorders in CI will be reviewed, in an attempt to explore the effect of mediating blood lipid levels on the prophylaxis and treatment of CI, thus providing a reference for its clinical management.

Peripheral inflammation as a potential mechanism and preventive strategy for perioperative neurocognitive disorder under general anesthesia and surgery.

General anesthesia, as a commonly used medical intervention, has been widely applied during surgical procedures to ensure rapid loss of consciousness and pain relief for patients. However, recent research suggests that general anesthesia may be associated with the occurrence of perioperative neurocognitive disorder (PND). PND is characterized by a decline in cognitive function after surgery, including impairments in attention, memory, learning, and executive functions. With the increasing trend of population aging, the burden of PND on patients and society's health and economy is becoming more evident. Currently, the clinical consensus tends to believe that peripheral inflammation is involved in the pathogenesis of PND, providing strong support for further investigating the mechanisms and prevention of PND.

Mechanism research on microRNA-669f-5p/deoxycytidylate deaminase axis mediating sevoflurane-induced cognitive dysfunction in aged mice.

OBJECTIVE: To investigate the role of the microRNA (miRNA)-669f-5p/deoxycytidylate deaminase (Dctd) axis in sevoflurane inducing cognitive dysfunction in aged mice. METHODS: Sixty-six C57BL/6J mice were used in the experiment model and were randomly divided into the sevoflurane group and the control group. The mice in the sevoflurane group were anesthetised with 3.4% sevoflurane, whereas those in the control group were air-treated for the same period. The study was then performed using bioinformatics sequencing, as well as in vitro and in vivo validation. RESULTS: The mice in the sevoflurane group showed significant cognitive impairments in terms of a decrease in both spatial learning and memory abilities. Experimental doses of miR-669f-5p agonist exhibited no obvious effect on cognitive function following sevoflurane inhalation, but inhibiting the expression of miR-669f-5p could alleviate the impairments. Based on the results of the bioinformatics sequencing, miR-669f-5p/Dctd and the toll-like receptor (TLR) signalling pathway could be the key miRNA, gene and pathway leading to postoperative cognitive dysfunction following sevoflurane inhalation. The aged mice showed significantly increased expression of miR-669f-5p in the hippocampus following sevoflurane inhalation, and upregulating/inhibiting its expression could increase/decrease TLR expression in the hippocampus. Furthermore, miR-669f-5p could reduce the expression of the Dctd gene by binding to its 3'untranslated region. CONCLUSION: The miR-669f-5p/Dctd axis plays an important role in sevoflurane inducing cognitive dysfunction in aged mice, providing a new direction for further development of therapeutic strategies concerning the prevention and treatment of cognitive dysfunction associated with sevoflurane anaesthesia.

Progress in the correlation of postoperative cognitive dysfunction and Alzheimer's disease and the potential therapeutic drug exploration.

Postoperative cognitive dysfunction (POCD) is a decrease in mental capacity that can occur days to weeks after a medical procedure and may become permanent and rarely lasts for a longer period of time. With the continuous development of research, various viewpoints in academic circles have undergone subtle changes, and the role of anesthesia depth and anesthesia type seems to be gradually weakened; Alzheimer's disease (AD) is a latent and progressive neurodegenerative disease in the elderly. The protein hypothesis and the synaptic hypothesis are well-known reasons. These changes will also lead to the occurrence of an inflammatory cascade. The exact etiology and pathogenesis need to be studied. The reasonable biological mechanism affecting brain protein deposition, neuroinflammation, and acetylcholine-like effect has a certain relationship between AD and POCD. Whereas there is still further uncertainty about the mechanism and treatment, and it is elusive whether POCD is a link in the continuous progress of AD or a separate entity, which has doubts about the diagnosis and treatment of the disease. Therefore, this review is based on the current common clinical characteristics of AD and POCD, and pathophysiological research, to search for their common points and explore the direction and new strategies for future treatment.