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Gut-brain axis and post-operative cognitive dysfunction:A multifactorial perspective on microbiota,inflammation,and cognitive health 认领 引用
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作者 Rhythm Joshi Nishkarsh Gupta +3 位作者 Anju Gupta Puneet Khanna Nishant Verma Simran Kaur 《World Journal of Gastrointestinal Pharmacology and Therapeutics》 2026年第1期92-102,共11页
Post-operative cognitive dysfunction(POCD)is a common but often overlooked issue,especially in older adults after surgery.This review looks into how the gut and brain are connected—a relationship known as the gut-bra... Post-operative cognitive dysfunction(POCD)is a common but often overlooked issue,especially in older adults after surgery.This review looks into how the gut and brain are connected—a relationship known as the gut-brain axis—and how tiny microbes living in our gut might influence our brain health during recovery.The gut microbiota helps produce important substances like short-chain fatty acids and neurotransmitters that play a key role in memory,mood,and brain function.Among these microbes,Akkermansia muciniphila stands out for supporting the gut lining,reducing inflammation,and balancing chemicals that affect cognition.Surgery,anesthesia,and antibiotics can disturb this balance,leading to“gut dysbiosis”,which may trigger brain inflammation and worsen POCD.By reviewing 11 carefully selected studies,this paper explores how restoring gut health—using probiotics like Akkermansia muciniphila or combinations like VSL#3—could be a promising way to protect the brain after surgery.Overall,these findings highlight a powerful connection between gut health and brain recovery,suggesting that personalized probiotic treatments might one day help improve mental outcomes in surgical patients.More clinical studies are needed,but the potential here is both exciting and hopeful. 展开更多
关键词 Gut-brain axis Post-operative cognitive dysfunction Gut microbiota Akkermansia muciniphila Neuroinflammation Short-chain fatty acids Gut dysbiosis Cognitive outcomes after surgery Probiotic intervention Microbiota-based targeted therapy
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Relationship between post-operative cognitive dysfunction and regional cerebral oxygen saturation and β-amyloid protein 认领 引用 被引量：26
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作者 Xi-ming LI Ming-tao SHAO +1 位作者 Jian-juan WANG Yue-lan WANG 《Journal of Zhejiang University-SCIENCE B》 SCIE CAS CSCD 2014年第10期870-878,共9页
Objective： To investigate the relationship between post-operative cognitive dysfunction（POCD） and regional cerebral oxygen saturation（rSO2） and β-amyloid protein（Aβ） in patients undergoing laparoscopic pancre... Objective： To investigate the relationship between post-operative cognitive dysfunction（POCD） and regional cerebral oxygen saturation（rSO2） and β-amyloid protein（Aβ） in patients undergoing laparoscopic pancreaticoduodenectomy. Methods： Fifty patients undergoing elective laparoscopic pancreaticoduodenectomy received five groups of neuropsychological tests 1 d pre-operatively and 7 d post-operatively, with continuous monitoring of rSO2 intra-operatively. Before anesthesia induction（t0）, at the beginning of laparoscopy（t1）, and at the time of pneumoperitoneum 120 min（t2）, pneumoperitoneum 240 min（t3）, pneumoperitoneum 480 min（t4）, the end of pneumoperitoneum（t5）, and 24 h after surgery, jugular venous blood was drawn respectively for the measurement of Aβ by enzyme-linked immunosorbent assay（ELISA）. Results： Twenty-one cases of the fifty patients suffered from POCD after operation. We found that the maximum percentage drop in rSO2（rSO2, %max） was significantly higher in the POCD group than in the non-POCD group. The rSO2, %max value of over 10.2% might be a potential predictor of neurocognitive injury for those patients. In the POCD group, the plasma Aβ levels after 24 h were significantly higher than those of pre-operative values（P〈0.01）. After 24 h, levels of plasma Aβ in the POCD group were significantly higher than those in the non-POCD group（P〈0.01）. Conclusions： The development of POCD in patients undergoing laparoscopic pancreaticoduodenectomy is associated with alterations of rSO2 and Aβ. Monitoring of rSO2 might be useful in the prediction of POCD, and Aβ might be used as a sensitive biochemical marker to predict the occurrence of POCD. 展开更多
关键词 Laparoscopic pancreaticoduodenectomy Regional cerebral oxygen saturation β-Amyloid protein Post-operative cognitive dysfunction
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Penehyclidine Hydrochloride Premedication Is Not Associated with Increased Incidence of Post-Operative Cognitive Dysfunction or Delirium:A Systemic Review and Meta-Analysis 认领 引用 被引量：5
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作者 Yuntai Yao Hua Ying +2 位作者 Nengxin Fang Yongbao Zhang Xin Yuan 《Chinese Medical Sciences Journal》 CAS CSCD 2020年第2期121-134,共14页
Objective Post-operative cognitive dysfunction(POCD)and post-operative delirium(POD)are two common post-operative cerebral complications.The current meta-analysis was to systematically review the effects of penehyclid... Objective Post-operative cognitive dysfunction(POCD)and post-operative delirium(POD)are two common post-operative cerebral complications.The current meta-analysis was to systematically review the effects of penehyclidine hydrochloride(PHC)on POCD and POD in surgical patients.Methods Electronic databases were searched to identify all randomized controlled trials comparing PHC with atropine/scopolamine/placebo on POCD and POD in surgical patients.Primary outcomes of interest included the incidences of POCD and POD;the secondary outcomes of interest included peri-operative minimental state examination(MMSE)scores.Two authors independently extracted peri-operative data,including patients'baseline characteristics,surgical variables,and outcome data.For dichotomous data(POCD and POD occurrence),treatment effects were calculated as odds ratio(OR)and 95%confidential interval(Cl).Each outcome was tested for heterogeneity,and randomized-effects or fixed-effects model was used in the presence or absence of significant heterogeneity.For continuous variables(MMSE scores),treatment effects were calculated as weighted mean difference(WMD)and 95%CI.Statistical significance was defined as P<0.05.Results Our search yielded 33 studies including 4017 patients.Meta-analysis showed that,the incidence of POCD in PHC group was comparable to that in saline group(OR=0.97;95%Ck 0.S8-1.64;P=0.92),scopolamine group(OR=0.78;95%CI:0.48-1.27;P=0.32)and atropine group(0R=1.20;95%Ch 0.86-1.67;P=0.29).The incidence of POD in PHC group was comparable to that in saline group(OR=1.53;95%CI:0.81-2.90;P=0.19)and scopolamine group(OR=0.53;95%CI:0.06-4.56;P=0.56),but higher than that in atropine group(OR=4.49;95%CI:1.34-15.01;P=0.01).Conclusions PHC premedication was not associated with increased incidences of POCD or POD as compared to either scopolamine or placebo. 展开更多
关键词 penehyclidine hydrochloride post-operative cognitive dysfunction post-operative delirium meta-analysis
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Modeling Post-Operative Cognitive Dysfunction in Zebrafish 认领 引用 被引量：1
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作者 Bill J. McElroy Julie L. Mustard +3 位作者 Syed Kamran Catherine P. Jung Katie L. Bakken Norbert W. Seidler 《Advances in Alzheimer's Disease》 CAS 2016年第3期126-141,共16页
Permanent post-operative cognitive dysfunction (POCD) is a grim outcome to an estimated 6% of elderly surgical patients. Volatile anesthetics impact neuronal tissue independent of effects attributed to the physical tr... Permanent post-operative cognitive dysfunction (POCD) is a grim outcome to an estimated 6% of elderly surgical patients. Volatile anesthetics impact neuronal tissue independent of effects attributed to the physical trauma of the surgery itself. While it is recognized that all aspects related to surgery may contribute to cognitive loss in some manner, the present paper focuses on the role of volatile anesthetics in promoting POCD. There is an increased risk of onset and progression of Alzheimer’s disease (AD) from POCD, implying that the neuropathogenesis between the two is similar. Human studies, being ethically limited in scope, require animal models as a substitute. While the literature using rodent models contains valuable information, we believe that the accessible and practical zebrafish will greatly enhance our further understanding of the molecular mechanism of POCD as it relates to AD. Disease genes and fundamental neurobehaviors of these teleost fish mirror those of mammals and humans, validating their use as a core research model for AD. Since the gradual senescence seen in zebrafish also resembles that found in humans, we numerically correlated the two lifespans, offering researchers a computational tool. Zebrafish, being aquatic animals, necessitates the use of miscible compounds, such as trifluoroethanol, whose anesthetic potency we are presenting. We also review the rodent and zebrafish literature relevant to POCD. Continued research with the leading-edge zebrafish unlocks the possibility that, in the future, perioperative intervention will prevent POCD. 展开更多
关键词 Zebrafish Post-Operative Cognitive Dysfunction Dementia Aging Anesthesia
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Xijiaqi Formula attenuates cognitive dysfunction by inhibiting neuroinflammation and promoting neuroplasticity in rats with chronic heart failure 认领 引用
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作者 Jie Chen Xuefen Wu +8 位作者 Qian Zhang Hongcai Shang Wanting Li Linnan Zhou Xinyu Chu Guiyang Xia Huan Xia Xiaohong Wei Sheng Lin 《Chinese Journal of Natural Medicines》 SCIE CAS CSCD 2026年第1期73-88,共16页
Chronic heart failure(CHF)impairs cognitive function.Xijiaqi Formula(XJQ),a traditional Chinese medicine(TCM)used clinically to treat CHF,demonstrates potential for improving cognition in CHF patients.However,its prec... Chronic heart failure(CHF)impairs cognitive function.Xijiaqi Formula(XJQ),a traditional Chinese medicine(TCM)used clinically to treat CHF,demonstrates potential for improving cognition in CHF patients.However,its precise mechanism in treating post-CHF cognitive dysfunction remains unclear.This study systematically investigates XJQ’s effects on post-CHF cognitive dysfunction and the underlying mechanisms.The components of XJQ were identified through liquid chromatography-mass spectrometry.CHF was induced in rats via ligation of the left anterior descending coronary artery,followed by six weeks of XJQ treatment.Cardiac function was evaluated through echocardiography and hemodynamic parameters,while cognitive function was assessed using Morris water maze(MWM)and open field tests(OFT).XJQ treatment enhanced both cardiac and cognitive functions in CHF rats.Network pharmacology identified 12 core active components of XJQ and indicated its effect on cognitive dysfunction involved regulating synapses,inflammation,and phosphodiesterase 4(PDE4)-dependent cyclic adenosine monophosphate(cAMP)signaling.XJQ inhibited microglial and astrocyte activation,decreased proinflammatory cytokines,and mitigated neuronal damage.Notably,XJQ promoted synaptic repair and dendritic growth by downregulating PDE4 and upregulating cAMP,protein kinase A(PKA),cAMP-response element binding protein(CREB),brain-derived neurotrophic factor(BDNF),PSD95,and synapsin I levels.Molecular docking and Bio-layer interferometry assays confirmed direct binding of quercetin,kaempferol,isorhamnetin,and darutoside to PDE4.In conclusion,XJQ alleviates neuroinflammation and enhances synaptic plasticity to improve cognitive dysfunction in CHF rats via the PDE4/cAMP/PKA/CREB signaling pathway.These findings provide valuable insight into the heart-brain axis. 展开更多
关键词 Xijiaqi Formula Cognitive dysfunction Chronic heart failure Synaptic plasticity Neuroinflammation PDE4
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Early-life gastrointestinal inflammation and the developing brain:Unravelling the pathways to long-term cognitive dysfunction 认领 引用
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作者 Mohammed Al-Beltagi Nermin Kamal Saeed +2 位作者 Yasser El-Sawaf Adel Salah Bediwy Reem Elbeltagi 《World Journal of Clinical Pediatrics》 2026年第2期1-31,共31页
The gut-brain axis(GBA)is a complex,bidirectional communication network critical to integrating central nervous system functions with gastrointestinal(GI)health.This review examines how disruptions to the GBA during t... The gut-brain axis(GBA)is a complex,bidirectional communication network critical to integrating central nervous system functions with gastrointestinal(GI)health.This review examines how disruptions to the GBA during the critical early-life developmental window–a period of rapid neurogenesis and microbial colonization–contribute to long-term neurocognitive and psychiatric vulnerabilities.Evidence from animal models demonstrates that early-life stress,antibiotics,and infection induce sustained neuro-inflammation and alter microglial function,leading to long-term behavioral and cognitive impairments in adulthood.Human studies corroborate these findings,revealing that severe early GI insults,such as necrotizing enterocolitis,confer a high risk(40%)of global neurodevelopmental impairment and specific attention deficits.Chronic inflammatory conditions similarly impact the central nervous system:A high burden of early severe enteric infection is an independent risk factor for diminished intelligence quotient(IQ)and executive function,while conditions like celiac disease and inflammatory bowel disease are associated with persistent deficits in attention,processing speed,memory,and executive function.These clinical outcomes are strongly linked to systemic inflammation[elevated interleukin-6,kynurenine-to-tryptophan(Kyn:Trp)ratio],micronutrient deficiencies(iron,vitamin B12,folate),and structural white matter changes in the brain.Furthermore,chronic GI disease imposes a significant psychiatric burden,with high comorbidity of anxiety and depression often mediating poor health-related quality of life,particularly in pediatric inflammatory bowel disease.The findings underscore the necessity for a shift in clinical practice:Chronic GI disease in early life must be recognized as a red flag for neurocognitive risk.We advocate for a multidisciplinary approach encompassing early neurodevelopmental follow-up for high-risk groups and routine screening for cognitive and emotional comorbidities.Future research must focus on long-term prospective cohorts,identifying precise mechanistic biomarkers(metabolomics,microbiome signatures),and conducting interventional trials targeting the GBA to mitigate these long-term functional consequences. 展开更多
关键词 Gut-brain axis Neurodevelopment Necrotizing enterocolitis Inflammatory bowel disease Celiac disease Cognitive dysfunction Microbiome
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Etiology and therapeutics for cognitive dysfunction in multiple system atrophy 认领 引用
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作者 Yasuo Miki Koichi Wakabayashi 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第8期3549-3550,共2页
Neurodegenerative disease is characterized by the presence of inclusion bodies containing abnormal toxic proteins in the central nervous system.Physiologicalα-synuclein exists in the form of a monomer or dimer at the... Neurodegenerative disease is characterized by the presence of inclusion bodies containing abnormal toxic proteins in the central nervous system.Physiologicalα-synuclein exists in the form of a monomer or dimer at the presynaptic nerve terminal.It serves as a key molecule to modulate endocytosis and exocytosis.However,under pathological conditions,α-synuclein adopts different conformations,being converted into toxic oligomers.The molecular weight ofα-synuclein oligomers ranges from 25 to 180 kDa,and they do not form filamentous aggregates ofα-synuclein.Subsequently,α-synuclein oligomers change to aggregates,including protofibrils and fibrils(Miki et al.,2022).This process has been implicated in the pathogenesis of neurodegenerative diseases collectively termed synucleinopathies,which include Parkinson’s disease,dementia with Lewy bodies,and multiple system atrophy(MSA). 展开更多
关键词 toxic oligomersthe neurodegenerative disease synuclein modulate endocytosis exocytosishoweverunder central nervous systemphysiological synuclein oligomers inclusion bodies cognitive dysfunction
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Dysfunction of hippocampal cells and its role in cognitive impairment 认领 引用
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作者 Jingwen Ye Lihong Zhou +9 位作者 Qiaohuizi Li Yuchen Huang Xiaoqin Wu Liusuyu Zhu Jie Zhu Jiahao Liu Dengsiyuan Gao Xia Chen Gang Chen Ying Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第8期3479-3495,共17页
Ischemic stroke has a higher survival rate and is more likely to result in cognitive impairment than hemorrhagic stroke.The primary pathological mechanism underlying cognitive impairment involves dysfunction of neural... Ischemic stroke has a higher survival rate and is more likely to result in cognitive impairment than hemorrhagic stroke.The primary pathological mechanism underlying cognitive impairment involves dysfunction of neural circuits and damage to specific brain regions.This review aims to investigate the role of the hippocampus in cognitive impairment following a stroke.A review of the literature suggests that the hippocampus is a metabolically active structure that is easily involved in various metabolic states,such as hypoxia and hypoglycaemia.The functional changes in hippocampal cells associated with poststroke cognitive impairment mainly manifest as neuronal apoptosis,impaired synaptic plasticity,and decreased neurogenesis.The primary pathological mechanism of poststroke cognitive impairment involves a complex cascade of reactions,including neuroinflammatory activation,bursts of oxidative stress,and neuronal apoptosis induced by mitochondrial dysfunction.Interventional drugs for cognitive impairment after cerebral ischemia include neuroprotective drugs,traditional Chinese medicines and their extracts,and stem cell therapies.Many of these drugs have unique advantages,including the inhibition of neuroinflammation,the prevention of apoptosis,and the promotion of neurogenesis.They hold great potential for the prevention and treatment of cognitive impairment following cerebral ischemia.However,most current studies are animal experiments,and relatively few clinical studies exist.In future research,emphasis should be placed on interventions for cognitive impairment following cerebral ischemia.These findings offer novel perspectives for the treatment of cognitive impairment after cerebral ischemia.Finally,the role of hippocampal cell dysfunction in other diseases associated with cognitive decline is briefly discussed.The aim of this review is to provide researchers with a comprehensive overview of the role of the hippocampus in cognitive impairment and its intervention strategies. 展开更多
关键词 apoptosis cerebral ischemia model cognitive decline hippocampal neurons hippocampus mitochondrial dysfunction neuroinflammation neuroprotection neurovascular unit poststroke cognitive impairment
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Overexpression of GluN2B Regulates Neuroinflammation through the BDNF/TrkB Signaling Pathway to Improve Postoperative Cognitive Dysfunction 认领 引用
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作者 Bohan Lin Wei Liu +1 位作者 Xiu Ni Fuyi Shen 《BIOCELL》 SCIE 2026年第6期164-184,共21页
Background:Postoperative cognitive dysfunction(POCD)is a common neurological complication in elderly patients.However,the mechanism by which glutamate ionotropic receptor NMDA type subunit 2B(GluN2B)contributes to POC... Background:Postoperative cognitive dysfunction(POCD)is a common neurological complication in elderly patients.However,the mechanism by which glutamate ionotropic receptor NMDA type subunit 2B(GluN2B)contributes to POCD development remains incompletely understood.This study aimed to investigate the effects of GluN2B overexpression on POCD improvement and elucidate its underlying molecular mechanisms.Methods:In vitro,lipopolysaccharide(LPS)was used to induce inflammation in mouse primary microglia,and a microglia-HT22 neuron co-culture system was established to simulate the neurotoxic environment.Overexpression and knockdown constructs for GluN2B and brain-derived neurotrophic factor(BDNF)were generated.Western blot,ELISA,immunofluorescence,and flow cytometry were employed to assess GluN2B expression,BDNFropomyosin receptor kinase B(TrkB)signaling proteins,microglial M1/M2 polarization markers,neuronal apoptosis,and synaptic markers.In vivo,an aged mouse POCD model was established to evaluate the effects of GluN2B overexpression on cognitive function,neuroinflammation,and neural injury markers.Results:LPS treatment downregulated GluN2B expression in microglia(4.71-fold,p<0.001),promoted polarization toward the pro-inflammatory M1 phenotype,and suppressed the BDNF/TrkB pathway.GluN2B overexpression significantly reversed these effects by inhibiting M1 polarization,enhancing anti-inflammatory M2 polarization,and activating BDNF/TrkB signaling.In the microglia-HT22 co-culture system,GluN2B overexpression markedly attenuated LPS-activated microglia-induced neuronal apoptosis(1.74-fold,p<0.001),intracellular Ca2+overload(1.94-fold,p<0.001),and synaptic protein loss in HT22 cells,whereas BDNF knockdown abolished these protective effects.In the aged POCD mouse model,GluN2B overexpression improved learning and memory performance and reduced neuronal apoptosis(1.92-fold,p<0.001)and histopathological damage in the prefrontal cortex.Conclusion:This study demonstrates that GluN2B overexpression activates the BDNF/TrkB pathway to reduce neuroinflammation,protect neurons and synapses,and ameliorate POCD symptoms in aged mice,providing a potential therapeutic target for POCD management. 展开更多
关键词 Glutamate ionotropic receptor NMDA type subunit 2B brain-derived neurotrophic factorropomyosin receptor kinase B pathway postoperative cognitive dysfunction microglial polarization neuroinflammation
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Effect of liposomal bupivacaine for iliac fascia block on postoperative cognitive dysfunction in patients with femoral neck fractures 认领 引用
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作者 Hui Liu Tong Jia +1 位作者 Shi-Chao Shuai Ji-Bo Zhao 《World Journal of Orthopedics》 2026年第5期132-141,共10页
BACKGROUND Neuroinflammation and circadian rhythm disruption caused by pain are the primary causes of postoperative cognitive dysfunction.We hypothesize that the administration of liposomal bupivacaine(LB)for fascia i... BACKGROUND Neuroinflammation and circadian rhythm disruption caused by pain are the primary causes of postoperative cognitive dysfunction.We hypothesize that the administration of liposomal bupivacaine(LB)for fascia iliaca compartment block(FICB)can alleviate pain intensity in patients with femoral neck fractures and reduce the incidence of postoperative cognitive dysfunction.AIM To explore the efficacy of LB for postoperative analgesia through FICB and their role in reducing cognitive dysfunction.METHODS Eighty patients aged≥65 years with femoral neck fractures were enrolled and randomly divided into the LB group and the control group according to different analgesic methods.The LB group received 0.266%LB solution via ultrasoundguided supra-inguinal FICB 1 day before surgery,while the control group did not receive FICB.Both groups were connected to a patient-controlled intravenous analgesia pump for postoperative analgesia.Comparisons were made between the two groups regarding resting and exercise visual analog scale(VAS)scores at 12 hours,24 hours,and 48 hours after surgery,the dosage of sufentanil in the analgesia pump,the mini-mental state examination(MMSE)scores 1 day before surgery and 1 day,3 days,and 7 days after surgery,the Pittsburgh Sleep Quality Index(PSQI)scores,postoperative blood glucose and serum cortisol levels,and related adverse reactions.RESULTS The mean arterial pressure was lower upon entering the operating room(T1)(P=0.009)and 12 hours after surgery(T3)(P=0.037)in the LB group than in the control group.The hazard ratio(HR)was lower at T1(P=0.000)and T3(P=0.000)in the LB group than in the control group.The blood glucose at T1(P=0.008),6 hours after surgery(P=0.000),T3(P=0.009),and 48 hours after surgery(T5)(P=0.000)were lower in the LB group than in the control group.The serum cortisol levels at T1(P=0.028)and T3(P=0.14)were lower in the LB group than in the control group.The resting and exercise VAS scores at T1(P=0.000),T3(P=0.002),1 day after surgery(P=0.000)and T5(P=0.000)were lower in the LB group than in the control group.The sufentanil dose was significantly lower in the LB group than in the control group(P=0.004).The MMSE scores at T1(P=0.000),3 days after surgery(P=0.000),7 days after surgery(P=0.000)were lower in the control group than in the LB group.The PSQI scores were lower in the LB group than in the control group(P=0.000).The incidences of postoperative nausea and vomiting(P=0.041)and excessive sleepiness(P=0.01)were significantly lower in the LB group than in the control group.CONCLUSION FICB with liposomal bupivacaine can provide continuous analgesia for patients undergoing femoral neck fracture surgery,significantly alleviating pain and anxiety,improving sleep quality,reducing opioid consumption,lowering the incidence of nausea and vomiting,and accelerating postoperative recovery. 展开更多
关键词 Liposomal bupivacaine Fascia iliaca compartment block Femoral neck fracture Postoperative cognitive dysfunction Postoperative pain Postoperative analgesia
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Surgical and anesthetic rewiring of the glymphatic system in postoperative cognitive dysfunction 认领 引用
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作者 Bandy Chen 《Neural Regeneration Research》 SCIE CAS CSCD 2026年第9期4271-4272,共2页
Postoperative cognitive dysfunction(POCD)is a condition characterized by a variety of neurological deficits,including memory deficits,difficulty with attention and executive function,and behavioral changes or delirium... Postoperative cognitive dysfunction(POCD)is a condition characterized by a variety of neurological deficits,including memory deficits,difficulty with attention and executive function,and behavioral changes or deliriumlike symptoms.These changes can be transient or long-lasting;however the exact mechanisms involved in POCD pathogenesis remain unclear.Well-established pathways that can contribute to POCD are neuroinflammation,blood-brain barrier disruption,and neurovascular dysfunction. 展开更多
关键词 neurovascular dysfunction anesthetic memory deficitsdifficulty postoperative cognitive dysfunction deliriumlike symptomsthese postoperative cognitive dysfunction pocd behavioral changes glymphatic system
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Systematic Review of Risk Factors for Cognitive Dysfunction and Nursing Intervention Models in Elderly Patients with Type 2 Diabetes Mellitus 认领 引用
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作者 Donglin Peng Jinyu Zhang Wei Zhao 《Journal of Clinical and Nursing Research》 2026年第5期345-353,共9页
Background:Type 2 diabetes mellitus(T2DM)is a common chronic metabolic disorder among the elderly,with a significantly higher incidence of cognitive dysfunction compared to the general population.Objective:To systemat... Background:Type 2 diabetes mellitus(T2DM)is a common chronic metabolic disorder among the elderly,with a significantly higher incidence of cognitive dysfunction compared to the general population.Objective:To systematically evaluate the risk factors for cognitive dysfunction and the efficacy of nursing interventions in elderly T2DM patients,providing a basis for early clinical identification and comprehensive care.Methods:Literature was retrieved from databases including China National Knowledge Infrastructure(CNKI),Wanfang Data Knowledge Service Platform,and PubMed,encompassing Chinese and English publications on risk factors and nursing interventions for cognitive dysfunction in elderly T2DM patients from 2024 to 2026.Two researchers independently conducted literature screening and data extraction.Results:A total of 17 studies were included.Independent risk factors for cognitive dysfunction in elderly T2DM patients included elevated glycated hemoglobin(HbA1c),prolonged diabetes duration,advanced age,high triglycerides,elevated low-density lipoprotein cholesterol(LDL-C),hypertension,and increased serum inflammatory markers.Regarding nursing intervention models,specialized community-based interventions and hyperbaric oxygen therapy combined with Baduanjin exercise effectively improved cognitive function.Conclusion:Clinical practice should emphasize glycemic control in elderly T2DM patients,strengthen early screening for high-risk populations,and adopt diversified nursing intervention approaches to delay cognitive decline. 展开更多
关键词 Type 2 diabetes mellitus Cognitive dysfunction Risk factors Nursing intervention Systematic review
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Recombinant chitinase-3-like protein 1 alleviates learning and memory impairments via M2 microglia polarization in postoperative cognitive dysfunction mice 认领 引用 被引量：1
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作者 Yujia Liu Xue Han +6 位作者 Yan Su Yiming Zhou Minhui Xu Jiyan Xu Zhengliang Ma Xiaoping Gu Tianjiao Xia 《Neural Regeneration Research》 SCIE CAS CSCD 2025年第9期2727-2736,共10页
Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life ... Postoperative cognitive dysfunction is a seve re complication of the central nervous system that occurs after anesthesia and surgery,and has received attention for its high incidence and effect on the quality of life of patients.To date,there are no viable treatment options for postoperative cognitive dysfunction.The identification of postoperative cognitive dysfunction hub genes could provide new research directions and therapeutic targets for future research.To identify the signaling mechanisms contributing to postoperative cognitive dysfunction,we first conducted Gene Ontology and Kyoto Encyclopedia of Genes and Genomes pathway enrichment analyses of the Gene Expression Omnibus GSE95426 dataset,which consists of mRNAs and long non-coding RNAs differentially expressed in mouse hippocampus3 days after tibial fracture.The dataset was enriched in genes associated with the biological process"regulation of immune cells,"of which Chill was identified as a hub gene.Therefore,we investigated the contribution of chitinase-3-like protein 1 protein expression changes to postoperative cognitive dysfunction in the mouse model of tibial fractu re surgery.Mice were intraperitoneally injected with vehicle or recombinant chitinase-3-like protein 124 hours post-surgery,and the injection groups were compared with untreated control mice for learning and memory capacities using the Y-maze and fear conditioning tests.In addition,protein expression levels of proinflammatory factors(interleukin-1βand inducible nitric oxide synthase),M2-type macrophage markers(CD206 and arginase-1),and cognition-related proteins(brain-derived neurotropic factor and phosphorylated NMDA receptor subunit NR2B)were measured in hippocampus by western blotting.Treatment with recombinant chitinase-3-like protein 1 prevented surgery-induced cognitive impairment,downregulated interleukin-1βand nducible nitric oxide synthase expression,and upregulated CD206,arginase-1,pNR2B,and brain-derived neurotropic factor expression compared with vehicle treatment.Intraperitoneal administration of the specific ERK inhibitor PD98059 diminished the effects of recombinant chitinase-3-like protein 1.Collectively,our findings suggest that recombinant chitinase-3-like protein 1 ameliorates surgery-induced cognitive decline by attenuating neuroinflammation via M2 microglial polarization in the hippocampus.Therefore,recombinant chitinase-3-like protein1 may have therapeutic potential fo r postoperative cognitive dysfunction. 展开更多
关键词 Chil1 hippocampus learning and memory M2 microglia neuroinflammation postoperative cognitive dysfunction(POCD) recombinant CHI3L1
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Impact of ambient temperature on postoperative cognitive dysfunction in elderly patients surgery:A seasonal comparison in tropical regions 认领 引用
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作者 Mi Liu Wen-Li Song +1 位作者 Hai-Jun Shen Yun-Mian Liu 《World Journal of Psychiatry》 SCIE 2025年第11期335-345,共11页
BACKGROUND To investigate whether seasonal differences in ambient temperature affect the incidence of early postoperative cognitive dysfunction(POCD)among elderly patients undergoing laparoscopic surgery in tropical r... BACKGROUND To investigate whether seasonal differences in ambient temperature affect the incidence of early postoperative cognitive dysfunction(POCD)among elderly patients undergoing laparoscopic surgery in tropical regions.Additionally,it explored the perioperative risk factors associated with early POCD following abdominal laparoscopic surgery.AIM To investigate the influence of seasonal differences in ambient temperature on POCD of elderly patients METHODS A total of 125 patients aged≥65 years from Hainan Province,China,who underwent laparoscopic surgery under general anesthesia with tracheal intubation,were enrolled. All patients completed the Mini-Mental State Examination one day before surgery and onpostoperative days 1, 3, and 7. A decline of ≥ 2 points from baseline was considered indicative of cognitivedysfunction. Serum levels of S100 calcium binding protein B and neuron-specific enolase were measured usingenzyme-linked immunosorbent assay at three time points: Preoperatively, immediately after extubation, and 24hours postoperatively. Perioperative clinical data were collected to identify potential risk factors for POCD.Propensity score matching (PSM) was performed (1:1, caliper = 0.03), resulting in 41 matched patient pairs betweenwinter and summer groups.RESULTSAfter PSM, baseline characteristics including age, gender, body mass index, education level, comorbidities, andsurgical variables were well balanced between groups. There were no significant differences in the incidence ofPOCD on postoperative days 1, 3, and 7 between patients undergoing laparoscopic surgery in winter vs summer.However, multivariable logistic regression revealed that surgical duration (day 1, P value = 0.049), advanced ageand elevated creatinine (day 3, P value = 0.044, P value = 0.008), and hypoalbuminemia (day 3, P value = 0.042;day7, P value = 0.015) were independently associated with early POCD.CONCLUSIONAmbient temperature differences between winter and summer in tropical regions did not significantly affect theincidence of early POCD in elderly patients undergoing laparoscopic surgery. Nonetheless, age, longer surgicalduration, elevated creatinine, and hypoalbuminemia emerged as key risk factors. These findings underscore theimportance of perioperative optimization to reduce the risk of POCD in elderly patients, regardless of seasonaltemperature variations. 展开更多
关键词 Tropical region Seasonal variation Ambient temperature Postoperative cognitive dysfunction Elderly Laparoscopic surgery Risk factors
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Troxerutin improves diabetic cognitive dysfunction by inhibiting mitochondrial fission mediated by transient receptor potential melastatin 7/calcineurin/dynamin-related protein 1ser637 认领 引用
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作者 Jie Li Ming Gao +5 位作者 Jia-Xin Wang Hong-Yan Li Pin Wang Fang Yuan Ai-Jing Liu Song-Yun Zhang 《World Journal of Diabetes》 SCIE 2025年第8期229-248,共20页
BACKGROUND Diabetic cognitive dysfunction(DCD)is one of the chronic complications of diabetes,but its mechanism is currently unknown.Studies have shown that mitochondrial fission mediated by calcium overload is an imp... BACKGROUND Diabetic cognitive dysfunction(DCD)is one of the chronic complications of diabetes,but its mechanism is currently unknown.Studies have shown that mitochondrial fission mediated by calcium overload is an important mechanism of DCD.Blocking calcium overload and restoring calcium homeostasis are key steps in treatment.Transient receptor potential melastatin 7(TRPM7)is a novel player in causing calcium overload.Our previous studies have shown that genetic silencing of TRPM7 in type 1 diabetic rats leads to significant improvements in cognitive function,but the specific mechanism remains unclear.Troxerutin,extracted from the flowers of Sophora japonica,is one of the derivatives of rutin and has been shown to have neuroprotective effects.However,its association with TRPM7 remains unclear.AIM To use animal and cellular models,we investigated whether TRPM7 mediated mitochondrial fission by upregulation of calcineurin(CaN)/dynamin-related protein 1(Drp1)ser637 in DCD,and whether Troxerutin improved DCD by inhibiting TRPM7-mediated mitochondrial division.METHODS In this study,we used db/db mice and hippocampal neuronal cell lines(HT22)treated with high-concentration glucose as our study subjects.We evaluated cognitive function using Morris water maze,novel object recognition tasks,and Nesting tests.We observed mitochondrial morphology using transmission electron microscopy and measured mitochondrial energy metabolism indicators using a spectrophotometer.We also detected mRNA and protein expression of TRPM7,CaN,p-Drp1ser637,caspase-3,B-cell lymphoma 2 associated X protein,and B-cell lymphoma 2 using quantitative real-time polymerase chain reaction,western blotting,and immunofluorescence.RESULTS In the db/db diabetic mice with cognitive dysfunction,as well as in hippocampal neurons exposed to high-concentration glucose,TRPM7 and CaN expression were upregulated,phosphorylated Drp1ser637expression was downregulated,and mitochondrial fission was increased.By modulating(inhibiting or overexpressing)TRPM7,it was further validated that TRPM7 activates the CaN/Drp1ser637pathway,resulting in an increase in mitochondrial fission and neuronal cell apoptosis.Troxerutin downregulated TRPM7/CaN/Drp1ser637,reduced mitochondrial fission,and improved DCD.CONCLUSION TRPM7 promotes mitochondrial fission via the CaN/Drp1ser637pathway.Troxerutin improves mitochondrial function and reduces neuronal damage by inhibiting this pathway,suggesting TRPM7 as a potential therapeutic target for DCD. 展开更多
关键词 Diabetic cognitive dysfunction Transient receptor potential melastatin 7 Mitochondrial fission Dynamin-related protein 1 Troxerutin Morris water maze Novel object recognition tasks Nesting tests
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FDA-approved cannabidiol[Epidiolex®]alleviates Gulf War Illness-linked cognitive and mood dysfunction,hyperalgesia,neuroinflammatory signaling,and declined neurogenesis 认领 引用
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作者 Maheedhar Kodali Leelavathi N.Madhu +8 位作者 Venkata Sai Vashishta Kolla Sahithi Attaluri Charles Huard Yogish Somayaji Bing Shuai Chase Jordan Xiaolan Rao Sanath Shetty Ashok K.Shetty 《Military Medical Research》 SCIE CAS CSCD 2025年第6期852-874,共23页
Background:Chronic Gulf War Illness(GWI)is characterized by cognitive and mood impairments,as well as persistent neuroinflammation and oxidative stress.This study aimed to investigate the efficacy of Epidiolex®,a... Background:Chronic Gulf War Illness(GWI)is characterized by cognitive and mood impairments,as well as persistent neuroinflammation and oxidative stress.This study aimed to investigate the efficacy of Epidiolex®,a Food and Drug Administration(FDA)-approved cannabidiol(CBD),in improving brain function in a rat model of chronic GWI.Methods:Six months after exposure to low doses of GWI-related chemicals[pyridostigmine bromide,N,N-diethyl-meta-toluamide(DEET),and permethrin(PER)]along with moderate stress,rats with chronic GWI were administered either vehicle(VEH)or CBD(20 mg/kg,oral)for 16 weeks.Neurobehavioral tests were conducted on 11 weeks after treatment initiation to evaluate the performance of rats in tasks related to associative recognition memory,object location memory,pattern separation,and sucrose preference.The effect of CBD on hyperalgesia was also examined.The brain tissues were processed for immunohistochemical and molecular studies following behavioral tests.Results:GWI rats treated with VEH exhibited impairments in all cognitive tasks and anhedonia,whereas CBD-treated GWI rats showed improvements in all cognitive tasks and no anhedonia.Additionally,CBD treatment alleviated hyperalgesia in GWI rats.Analysis of hippocampal tissues from VEH-treated rats revealed astrocyte hypertrophy and increased percentages of activated microglia presenting NOD-,LRR-and pyrin domain-containing protein 3(NLRP3)complexes as well as elevated levels of proteins involved in NLRP3 inflammasome activation and Janus kinase/signal transducers and activators of the transcription(JAK/STAT)signaling.Furthermore,there were increased concentrations of proinflammatory and oxidative stress markers along with decreased neurogenesis.In contrast,the hippocampus from CBD-treated GWI rats displayed reduced levels of proteins mediating the activation of NLRP3 inflammasomes and JAK/STAT signaling,normalized concentrations of proinflammatory cytokines and oxidative stress markers,and improved neurogenesis.Notably,CBD treatment did not alter the concentration of endogenous cannabinoid anandamide in the hippocampus.Conclusions:The use of an FDA-approved CBD(Epidiolex®)has been shown to effectively alleviate cognitive and mood impairments as well as hyperalgesia associated with chronic GWI.Importantly,the improvements observed in rats with chronic GWI in this study were attributed to the ability of CBD to significantly suppress signaling pathways that perpetuate chronic neuroinflammation. 展开更多
关键词 Gulf War Illness(GWI) Anhedonia Activated microglia Cannabidiol(CBD) Chronic neuroinflammation Cognition Hippocampal neurogenesis Inflammasomes Janus kinase/signal transducers and activators of the transcription(JAK/STAT)signaling Memory dysfunction NOD- LRR-and pyrin domain-containing protein 3(NLRP3)inflammasomes Oxidative stress
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Construction of a risk prediction model for postoperative cognitive dysfunction in colorectal cancer patients 认领 引用 被引量：1
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作者 Zhen-Ping Zheng Yong-Guo Zhang +3 位作者 Ming-Bo Long Kui-Quan Ji Jin-Yan Peng Kai He 《World Journal of Gastrointestinal Surgery》 SCIE 2025年第4期221-232,共12页
BACKGROUND Colorectal cancer(CRC)is one of the most prevalent and lethal malignant tumors worldwide.Currently,surgical intervention was the primary treatment modality for CRC.However,increasing studies have revealed t... BACKGROUND Colorectal cancer(CRC)is one of the most prevalent and lethal malignant tumors worldwide.Currently,surgical intervention was the primary treatment modality for CRC.However,increasing studies have revealed that CRC patients may experience postoperative cognitive dysfunction(POCD).AIM To establish a risk prediction model for POCD in CRC patients and investigate the preventive value of dexmedetomidine(DEX).METHODS A retrospective analysis was conducted on clinical data from 140 CRC patients who underwent surgery at the People’s Hospital of Qian Nan from February 2020 to May 2024.Patients were allocated into a modeling group(n=98)and a validation group(n=42)in a 7:3 ratio.General clinical data were collected.Additionally,in the modeling group,patients who received DEX preoperatively were incorporated into the observation group(n=54),while those who did not were placed in the control group(n=44).The incidence of POCD was recorded for both cohorts.Data analysis was performed using statistical product and service solutions 20.0,with t-tests orχ2 tests employed for group comparisons based on the data type.Least absolute shrinkage and selection operator regression was applied to identify influencing factors and reduce the impact of multicollinear predictors among variables.Multivariate analysis was carried out using Logistic regression.Based on the identified risk factors,a risk prediction model for POCD in CRC patients was developed,and the predictive value of these risk factors was evaluated.RESULTS Significant differences were observed between the cognitive dysfunction group and the non-cognitive dysfunction group in diabetes status,alcohol consumption,years of education,anesthesia duration,intraoperative blood loss,intraoperative hypoxemia,use of DEX during surgery,intraoperative use of vasoactive drugs,surgical time,systemic inflammatory response syndrome(SIRS)score(P<0.05).Multivariate Logistic regression analysis identified that diabetes[odds ratio(OR)=4.679,95%confidence interval(CI)=1.382-15.833],alcohol consumption(OR=5.058,95%CI:1.255-20.380),intraoperative hypoxemia(OR=4.697,95%CI:1.380-15.991),no use of DEX during surgery(OR=3.931,95%CI:1.383-11.175),surgery duration≥90 minutes(OR=4.894,95%CI:1.377-17.394),and a SIRS score≥3(OR=4.133,95%CI:1.323-12.907)were independent risk factors for POCD in CRC patients(P<0.05).A risk prediction model for POCD was constructed using diabetes,alcohol consumption,intraoperative hypoxemia,non-use of DEX during surgery,surgery duration,and SIRS score as factors.A receiver operator characteristic curve analysis of these factors revealed the model’s predictive sensitivity(88.56%),specificity(70.64%),and area under the curve(AUC)(AUC=0.852,95%CI:0.773-0.919).The model was validated using 42 CRC patients who met the inclusion criteria,demonstrating sensitivity(80.77%),specificity(81.25%),and accuracy(80.95%),and AUC(0.805)in diagnosing cognitive impairment,with a 95%CI:0.635-0.896.CONCLUSION Logistic regression analysis identified that diabetes,alcohol consumption,intraoperative hypoxemia,non-use of DEX during surgery,surgery duration,and SIRS score vigorously influenced the occurrence of POCD.The risk prediction model based on these factors demonstrated good predictive performance for POCD in CRC individuals.This study offers valuable insights for clinical practice and contributes to the prevention and management of POCD under CRC circumstances. 展开更多
关键词 Colorectal cancer Postoperative Cognitive dysfunction Anesthesia Risk prediction model Dexmedetomidine Preventive value
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Inhibition of the microglial voltage-gated proton channel 1 channel ameliorates diabetes-associated cognitive dysfunction by regulating axon demyelination 认领 引用 被引量：1
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作者 Chun-Yu Li Shu-Jun Zhang +3 位作者 Jia-Lu Xu Yan Yang Zhi-Xuan Zeng De-Lin Ma 《World Journal of Psychiatry》 SCIE 2025年第3期288-301,共14页
BACKGROUND Diabetes is associated with increased cognitive decline and dementia due to the loss of myelinated nerve fiber function,which is linked to oligodendrocyte dysfunction.The voltage-gated proton channel 1(Hv1)... BACKGROUND Diabetes is associated with increased cognitive decline and dementia due to the loss of myelinated nerve fiber function,which is linked to oligodendrocyte dysfunction.The voltage-gated proton channel 1(Hv1)is important for the cellular proton extrusion machinery.However,its role in regulating diabetesinduced cognitive dysfunction is unclear.AIM To investigate the role of Hv1 in cognitive impairment induced by diabetes and its potential mechanisms,focusing on neuroinflammation,oligodendrocyte apoptosis,and axonal demyelination.METHODS A diabetes model was established by administering a high-fat diet and streptozotocin injections in mice.Hv1 knockout(KO)and wild-type mice were used to evaluate cognitive function via behavioral tests and neuroinflammation using immunofluorescence.Oligodendrocyte apoptosis was assessed with the terminal deoxynucleotidyl transferase deoxyuridine triphosphate nick-end labeling assay, and axonal demyelination wasanalyzed using electron microscopy.RESULTSHv1 expression was significantly increased in the corpus callosum of diabetic mice. Hv1 KO alleviated cognitiveimpairment, reduced oligodendrocyte apoptosis, and decreased the expression of inflammatory factors, includinginterleukin-1 and tumor necrosis factor-α, in diabetic mice. Electron microscopy revealed a reduction in myelinthickness and an increased g-ratio in diabetic mice, which were reversed by Hv1 KO.CONCLUSIONHv1 plays a role in diabetes-induced cognitive dysfunction by modulating neuroinflammation and myelinintegrity. Hv1 KO demonstrates therapeutic potential in mitigating diabetes-related cognitive decline andassociated complications. 展开更多
关键词 Diabetes Cognitive dysfunction Voltage-gated proton channel 1 Neuroinflammation Myelin regeneration
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The Role of Central Inflammation in Postoperative Cognitive Dysfunction 认领 引用 被引量：1
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作者 Wenyuan Zhang Fang Yan 《Journal of Clinical and Nursing Research》 2025年第2期35-39,共5页
Postoperative cognitive dysfunction is a typical complication,which can be referred to as POCD.This complication is common in elderly patients.Among them,POCD is mainly manifested in the function of patients with atte... Postoperative cognitive dysfunction is a typical complication,which can be referred to as POCD.This complication is common in elderly patients.Among them,POCD is mainly manifested in the function of patients with attention deficit and memory reduction after surgery,among which serious patients are prone to personality change,which affects their social behavior ability.In the context of the current era,the cause of POCD is not clear,combined with the results of most studies,it is found that central nervous inflammation,is a key factor affecting POCD.From the perspective of central inflammation,this paper analyzes the relationship between central inflammation and POCD,and discusses the mechanism of action,aiming at effectively preventing and treating POCD and providing a reference for subsequent research in related fields. 展开更多
关键词 Central inflammation Postoperative cognitive dysfunction Effects
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Dihydromyricetin reverses cognitive dysfunction in type 2 diabetic rats via inhibition of the JNK-ERS axis 认领 引用
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作者 Huijie Lv Jun Peng +3 位作者 Xu Huang Tuo Xu Tianchen Zhang Hongyan Ling 《Journal of Chinese Pharmaceutical Sciences》 CAS CSCD 2025年第11期1003-1023,共21页
Recent studies have demonstrated that dihydromyricetin(DHM)exerts a protective effect against central nervous system injury.Building on these findings,the present study aimed to investigate whether DHM could ameliorat... Recent studies have demonstrated that dihydromyricetin(DHM)exerts a protective effect against central nervous system injury.Building on these findings,the present study aimed to investigate whether DHM could ameliorate cognitive deficits in a type 2 diabetes mellitus(T2DM)rat model,and to explore whether this effect involved inhibition of the JNK signaling pathway and suppression of endoplasmic reticulum stress(ERS).To establish the T2DM model,Sprague Dawley(SD)rats were fed a high-fat,high-sugar diet in combination with a single intraperitoneal injection of streptozotocin(STZ).Fasting blood glucose levels were measured from tail vein samples,and cognitive performance was evaluated using the Morris water maze(MWM)and Y-maze tests.Following behavioral assessments,the animals were sacrificed by cervical dislocation,and hippocampal tissues were collected for further analysis.Histological examination using hematoxylin-eosin(H&E)staining was performed to assess hippocampal neuronal damage.Western blotting(WB)analysis was employed to quantify the expression of pro-apoptotic protein Bax and anti-apoptotic protein Bcl-2,while ELISA was conducted to measure levels of phosphorylated tau(p-tau)and amyloid-β(Aβ)in the hippocampus.After 12 weeks of oral administration of DHM(250 mg/kg/d),relevant biomarkers were re-evaluated to determine the compound's impact on cognitive function and hippocampal integrity.Additionally,rats from each group received intracerebroventricular injections of various pharmacological agents,namely,TUDCA(an ERS inhibitor),STZ,SP600125(a JNK inhibitor),and anisomycin(AMY,a JNK activator).WB analysis was further conducted to assess the expression of JNK,phosphorylated JNK(p-JNK),and ERS-associated proteins Bip and p-PERK in hippocampal tissue.The results confirmed that combining a high-fat,high-sugar diet with low-dose STZ injection for 4 weeks effectively established a T2DM model.Compared with the control group,T2DM rats exhibited significant cognitive deficits,increased neuronal apoptosis in the hippocampus,and elevated hippocampal levels of p-tau and Aβ.Notably,DHM treatment markedly reversed these pathological changes in T2DM rats,whereas it had no significant effects on control animals.Moreover,administration of TUDCA and SP600125 similarly mitigated cognitive impairment,neuronal apoptosis,and the accumulation of p-tau and Aβin diabetic rats.Conversely,activation of ERS and JNK signaling using tunicamycin(TUN)and AMY,respectively,resulted in exacerbated cognitive decline,increased neuronal apoptosis,and higher levels of p-tau and Aβ.In conclusion,these findings suggested that DHM effectively alleviated cognitive dysfunction in T2DM rats,potentially through the inhibition of JNK signaling and subsequent attenuation of ERS,thereby reducing neuronal apoptosis and the pathological accumulation of p-tau and Aβin the hippocampus. 展开更多
关键词 Dihydromyricetin Type 2 diabetes Cognitive dysfunction JNK signaling Endoplasmic reticulum stress
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