Mucosal healing (MH) has established as a long-term therapeutic goal for inflammatory bowel disease (IBD). Regenerative Islet-derived Protein 1α (reg1α) was reported to be closely related to gastrointestinal mucosal injury; however, its potential in monitoring MH remains unexplored.

Serum reg1α levels were quantified in 156 consecutive IBD patients (January 2021-December 2023) and stratified by endoscopic findings into MH (n = 136) and non-mucosal healing (NMH) groups. Diagnostic performance of reg1α was evaluated and compared to C-reactive protein (CRP) using receiver operating characteristic analysis.

A total of 136 patients (85 with CD and 51 with UC) were finally included. Serum reg1α levels were significantly correlated with endoscopic activity. Patients in NMH group demonstrating markedly higher reg1α levels than those in MH group (92.6 vs. 55.5 ng/ml, p < 0.001). In UC, reg1α outperformed CRP in sensitivity (82.4% vs. 55.9%, p = 0.012) and accuracy (80.4% vs. 70.6%, p = 0.001) for monitoring MH. This superiority persisted in UC subgroups with non-or mild clinical symptoms. Combined index (reg1α + CRP) and multivariate model (incorporating clinical indices, reg1α and CRP) also enhanced sensitivity and accuracy over CRP alone in UC (all p < 0.05). However, reg1α showed no significantly higher efficacy in monitoring NMH compared to CRP in CD. In CRP-normal patients, patients with NMH had higher reg1α levels than those with MH in UC (77.6 vs. 49.8 ng/ml, p = 0.018), but not in CD.

Reg1α represents as a novel and sensitive biomarker of endoscopic disease activity in patients with UC, even in patients with non- or mild clinical symptoms or normal CRP levels.

Observational studies have demonstrated associations between autoimmune thyroid disease and both mood disorders and dementia, but the direction of causality has not been established.

We employed bidirectional, two-sample Mendelian randomization analyses to assess the causal links between autoimmune thyroid disease (Graves' disease and autoimmune thyroiditis), and mood disorders (major depressive disorder and bipolar disorder) as well as dementia (Alzheimer's disease and dementia with Lewy bodies). We obtained Genome-Wide Association Study data from the Finngen database and IEU Open GWAS. For statistical analysis, we utilized several robust methods inverse variance weighted, MR-Egger, weighted median, simple mode and weighted mode. Sensitivity analyses are performed to detect potential horizontal pleiotropy, and to exclude any outlier data points that could skew our results.

Gene-proxy for Graves' disease was associated with an increased risk of major depressive disorder (P-value = 0.02), whereas gene-proxy for autoimmune thyroiditis was linked to a greater risk of bipolar disorder (P-value = 0.043). The levels of pleiotropy and heterogeneity among genetic variants suggest bias is unlikely, leave-one-out test confirmed a robust correlation. No indication that mood disorders influence the risk of autoimmune thyroid disease, and no evidence of a causal relationship between autoimmune thyroid disease and dementia.

Graves' disease is associated with heightened risk of major depressive disorder, and autoimmune thyroiditis is correlated with increased risk of bipolar disorder.

To explore the relationship between body mass index (BMI) and its changes in relation to cognitive decline across different cognitive status, while also examining the role of the APOE genotype in these associations.

A total of 23 255 individuals from the National Alzheimer's Coordinating Center (NACC) were analysed using multivariable logistic and Cox regression to assess BMI and its variability in relation to cognitive decline. Subgroup analyses were conducted to explore how APOE genotype interacts with BMI and cognitive decline.

Compared to individuals with normal cognition and normal BMI, being underweight was associated with a higher risk of developing MCI (HR 3.065, 95% CI: [1.156-8.126]) and dementia (HR 4.057, 95% CI: [1.433-11.483]). Over the 4.07-year follow-up, 9171 individuals experienced cognitive decline. Longitudinal analysis revealed that being overweight or obese was linked to a lower risk of cognitive decline across different cognitive status, including impaired not MCI, MCI and dementia, but had no effect on those with normal cognition. Additionally, compared to stable BMI, the hazard ratios (95% CI) for developing dementia were 2.336 (2.128-2.565) and 2.338 (2.119-2.581) for annual BMI gain or loss greater than 5%. However, different APOE genotypes may influence the effect of BMI and BMI variability on cognitive decline.

This research supports the 'obesity paradox' and highlights the critical role of APOE in modulating BMI's influence on cognitive health.

Stroke ranks as the second leading cause of mortality and the third leading cause of disability globally. Post-stroke cognitive impairment (PSCI) is a prevalent complication following acute ischemic stroke, imposing substantial burdens on patients, families, and society. This study aimed to explore the potential of circulating immune-inflammatory markers as predictors of PSCI.

Conducted as a prospective observational cohort study from June 2023 to August 2024 at the Affiliated Drum Tower Hospital, Medical School of Nanjing University, it included patients experiencing their first acute ischemic stroke within 72 h of symptom onset. Cognitive assessments were conducted 7 to 10 days post-stroke using the Montreal Cognitive Assessment (MoCA), with scores below 23 indicating PSCI.

A total of 146 patients meeting the inclusion criteria were recruited, with 71 patients exhibiting PSCI during the acute phase of stroke. Compared to patients in the post-stroke no cognitive impairment (PSNCI) group, those with PSCI demonstrated significantly elevated peripheral blood neutrophil-to-lymphocyte ratio (NLR), globulin-to-lymphocyte ratio (GLR), and C-reactive protein-to-lymphocyte ratio (CLR), while the lymphocyte-to-monocyte ratio (LMR) was notably reduced (all p < 0.05). Both univariate and multivariate logistic regression analyses identified GLR as independently associated with PSCI. After adjusting for common clinical variables, the odds ratio (OR) for the highest tertile of GLR compared to the lowest was 6.20 (95% CI, 2.10-18.33; p = 0.001). The optimal GLR cutoff was 18.22, with a sensitivity of 62.0%, specificity of 78.7%, and an area under curve (AUC) of 0.726.

This study indicates that elevated circulating GLR levels during the acute phase post-stroke onset are an independent risk factor for early-onset PSCI, even after adjusting for clinically relevant variables.

Emerging evidence indicates that inflammatory bowel disease (IBD) and dementia may share underlying pathological mechanisms and risk factors. However, the association between a prior IBD diagnosis and the subsequent risk of dementia remains largely unexplored. We conducted a comprehensive search of PubMed, Embase, and the Cochrane Library up to February 4, 2025, without language restrictions. Two reviewers independently extracted data and evaluated methodological quality and risk of bias. Observational studies comparing dementia risk in IBD and non-IBD populations were included. Pooled effect estimates for odds ratios (OR) were calculated using random-effects models. A total of 10 population-based studies, involving 7,895,339 participants (269,387 with IBD), were included. Meta-analysis of eight studies showed a significant association between IBD and dementia risk (OR 1.17, 95% CI: 1.08-1.27, P = 0.0001). However, IBD was not associated with an increased risk of Alzheimer's disease (AD) (OR 1.15, 95% CI: 0.98-1.36, P = 0.09). Stratified analysis by IBD type revealed a positive association between both ulcerative colitis (UC) and Crohn's disease (CD) and dementia risk (UC: OR 1.15, 95% CI: 1.05-1.25, P = 0.002, I² = 81%; CD: OR 1.26, 95% CI: 1.11-1.43, P = 0.0003, I² = 53%). This study identifies a significant correlation between IBD and dementia, suggesting that IBD patients have an elevated risk of developing dementia. However, current evidence is insufficient to establish a causal relationship. Further research should explore whether effective IBD treatments can mitigate this risk and elucidate the underlying pathophysiological mechanisms connecting these conditions.

Cognitive impairment poses significant challenges for aging populations. Systemic inflammation, a hallmark of rheumatoid arthritis (RA), has been implicated in neurodegeneration through mechanisms including blood-brain barrier disruption, microglial activation, and cytokine-mediated neuronal damage. This review examines the potential impact of disease-modifying antirheumatic drugs (DMARDs) on cognitive function in RA, focusing on the inflammatory pathways linking systemic inflammation to neuroinflammation and cognitive decline. DMARDs, categorized into conventional synthetic (csDMARDs), biologic (bDMARDs), and targeted synthetic (tsDMARDs) classes, modulate immune responses through distinct mechanisms. Evidence suggests that DMARDs, particularly bDMARDs targeting proinflammatory cytokines such as TNF-α and IL-6, may mitigate neuroinflammatory processes and preserve cognitive function. However, the cognitive impact of csDMARDs such as methotrexate is complex, with conflicting reports regarding its role in vascular dementia. Emerging therapies such as Janus kinase inhibitors (JAK-i) offer promise in modulating central inflammation, though clinical evidence remains limited. While some studies highlight protective effects of DMARDs against dementia, findings are inconsistent, hindered by heterogeneity in study design, patient demographics, and cognitive assessment methods. This review underscores the need for personalized treatment strategies, integrating RA management with cognitive health considerations. Future research should prioritize robust, prospective studies with long-term follow-up, incorporating neuroimaging and biomarker analysis to elucidate the mechanisms underpinning DMARD-associated cognitive outcomes. A better understanding of the involved inflammatory pathways in RA and the potential effects of DMARDs could lead to improved therapeutic approaches, enhancing quality of life for patients with RA and potentially benefiting broader strategies in preventing or treating dementia.

Mild cognitive impairment (MCI) is a transitional stage to dementia, Alzheimer's disease being a major cause. Although amyloid beta-positive (Aβ+) MCI has been well-characterized, Aβ-negative (Aβ-) MCI has not. This study compared the comprehensive clinical and behavioral characteristics of Aβ+ and Aβ- MCI in a large multi-center cohort to better understand the heterogeneity of MCI, and to identify contributing factors to cognitive impairment.

A total of 686 MCI participants were included. Aβ positivity was determined using Aβ positron emission tomography imaging with a direct conversion Centiloid cutoff value of 25.5. Standardized assessment and questionnaires were used to collect a wide range of clinical information, including vascular risk factors, cognition, daily living function, neuropsychiatric symptoms, and lifestyle behavior. Groups were compared using independent t-tests and χ2 tests.

Aβ+ participants (n=406) were older, predominantly female, and more likely to be ApoE4 carriers. In contrast, Aβ- participants (n=280) showed higher vascular risk factors, including diabetes, elevated body mass index, and higher C-reactive protein levels. Aβ+ participants exhibited worse global cognition and functional decline, with a higher prevalence of delusions and appetite disturbances. Meanwhile, Aβ- participants reported greater social engagement, but poorer sleep quality.

This study highlights the distinct clinical and lifestyle profiles of Aβ+ and Aβ- MCI, illuminating the heterogeneity of MCI and its underlying factors in the Korean population.

Rheumatoid arthritis (RA) has been linked to an increased risk of dementia, yet little is known about how RA affects the progression of cognitive impairment and the risk of mortality in people with dementia. We aimed to investigate whether RA is linked to an accelerated cognitive decline and a higher risk of all-cause mortality in patients with dementia.

We conducted a propensity score-matched register-based cohort study based on the Swedish Registry for Cognitive/Dementia Disorders-SveDem. Patients diagnosed with dementia and registered in SveDem between May 1, 2007, and October 16, 2018, were included. The main outcome for the study was cognitive decline, measured by Mini-Mental State Examination (MMSE) score changes over years. The secondary outcome was all-cause death. We used mixed-effects models to examine the association between RA and cognitive decline, and Cox proportional hazards models to investigate the risk of all-cause mortality. We also conducted subgroup analyses to explore the potential effects of sociodemographic, baseline MMSE, comorbidities, and the use of dementia medications on the association between RA and outcomes.

We included 1,685 dementia patients with RA (mean [SD] age, 79.9 [6.7] years; 73.4% were women) and 5,055 dementia patients with non-RA (80.1 [7.5] years; 73.1% were women). The median follow-up was 2.9 years (interquartile range, 1.5-4.6 years) for non-RA and 2.6 years (interquartile range, 1.4-4.2 years) for RA. In total, 111,266 MMSE measurements were available for analysis. Compared with non-RA patients, patients with RA presented faster cognitive decline (β = -0.24 points/y; 95% CI -0.38 to -0.10) and an increased risk of death (hazard ratio 1.15; 95% CI 1.06-1.24). In subgroup analysis, significant interactions were observed between RA and baseline MMSE scores as well as living conditions regarding cognitive decline (p for interaction <0.05).

We identified a worse cognitive function and an increased mortality risk in dementia patients with RA compared with non-RA. However, we lacked information on the duration of RA before the onset of dementia and on disease activity, which could influence our findings. Further studies are needed to validate these results in comparable populations.

Elevated worry is an early indicator of cognitive decline in older adults. Worry has been linked to pro-inflammatory processes though the exact relations between worry, inflammation, and cognition in older adults with amnestic mild cognitive impairment (aMCI) remain unexplored. The present study studied the association of worry with proteomic biomarkers of inflammation and cognition.

Participants include 66 community-dwelling older adults with amnestic mild cognitive impairment (aMCI). Inflammation was analyzed using the modified aptamer-based assay SomaScan Platform. Primary analyses consisted of two hierarchical regression models with mean-centered worry and inflammation as independent variables and age as covariate. Composite scores of executive function and processing speed were entered as the dependent variable in separate models.

Results indicate a significant interaction between worry and placental growth factor (PIGF) on processing speed, such that worry intensifies the inverse relationship of PIGF and processing speed. Worry did not interact with PIGF to predict executive functioning.

Findings indicate an important moderating role of worry in the association of pro-inflammatory PIGF and processing speed. Results suggest that older adults with cognitive impairment may be more susceptible to the indirect impact of worry and expands emerging research on the role of PIGF in cognitive impairment.

Social frailty, a multidimensional construct encompassing various social behaviors, resources, and needs, significantly impacts cognitive health in older adults. Despite existing studies linking specific social factors to cognitive function, the association between social frailty and long-term cognitive trajectories remains underexplored. This study aims to evaluate the longitudinal association between social frailty and trajectory of cognitive function in dementia-free older adults.

This prospective cohort study used data from the National Health and Aging Trends Study (NHATS). Social frailty was assessed using the Makizako Social Frailty Index. According to the presence of social components, individuals were categorized into social frailty (≥ 2), pre-social frailty (1), and robust (0), respectively. Cognitive function was annually evaluated through memory, orientation, and executive function tests from 2011 to 2018. Mixed-effects linear models were employed to assess the associations between social frailty and changes in global and domain-specific cognitive function, adjusting for relevant covariates.

In this study, 4956 dementia-free older adults (mean age 76.57 [7.41]) with complete at least 2 times of cognitive tests were included. Compared with the robust, social frailty was associated with significantly faster decline in global cognitive function (β = -0.041, 95% CI [-0.047, -0.036] z score per year) and domain-specific cognitive function (βmemory = -0.045, 95% CI [-0.055, -0.036] z score per year; βorientation = -0.027, 95% CI [-0.034, -0.020] z score per year; βexecutive = -0.042, 95% CI [-0.053, -0.032] z score per year) over the follow-up. Additionally, pre social frailty was associated with significantly faster decline in global cognitive function (β = -0.016, 95% CI [-0.021, -0.012] z score per year), memory function (β= -0.045, 95% CI [-0.055, -0.036] z score per year), and orientation function (β= -0.027, 95% CI [-0.034, -0.020] z score per year) over the follow-up.

Social frailty is associated with faster decline in cognition in older adults, underscoring the necessity for enhanced social support and engagement to mitigate cognitive deterioration in vulnerable populations.

Multimorbidity is associated with increased risk of dementia, but previous estimation of the joint contribution of constituent conditions to dementia incidence did not model additive contributions or temporal proximity in the sequential onset of conditions.

Data were analyzed from 9944 Health and Retirement Study participants and Medicare fee-for-service beneficiaries, ages 68-99, without Alzheimer's disease and related dementias (ADRD) at baseline, from 1998-2016. ADRD and chronic condition were encoded using validated claims algorithms. We estimated the absolute contribution of eight conditions to ADRD with the longitudinal extension of the average attributable fraction (LE-AAF).

Hypertension, acute myocardial infarction, atrial fibrillation, diabetes, heart failure, ischemic heart disease, stroke, and arthritis additively accounted for 71.8% (95% confidence interval [CI]: 62.9%-79.1%) of ADRD incident cases based on LE-AAF.

Our findings suggest that multimorbidity plays a pivotal role in ADRD incidence. Targeting constituents of a cardiovascular path to dementia may contribute most to lowering dementia risk.

Most dementia cases (71.8%) were attributable to eight chronic conditions. Hypertension was the largest contributor to dementia risk. Confidence intervals were smallest for constituents of a cardiovascular path to dementia. Longitudinal extension of the average attributable fractions (LE-AAFs) explicitly consider longitudinal patterns of comorbidities. Acute myocardial infarction did not contribute significantly to dementia incidence.

Gliomas are the most frequent, heterogeneous group of tumors arising from glial cells, characterized by difficult monitoring, poor prognosis, and fatality. Tissue biopsy is an established procedure for tumor cell sampling that aids diagnosis, tumor grading, and prediction of prognosis.

We studied and compared the levels of liquid biopsy markers in patients with different grades of glioma. Also, we tried to prove the potential association between glioma and specific blood group antigens.

78 patients were found, among whom the maximum percentage with glioblastoma had blood group O+ (53.8%). The second highest frequency had blood group A+ (20.4%), followed by B+ (9.0%) and A- (5.1%), and the least with O-. Liquid biopsy biomarkers included Alanine Aminotransferase (ALT), Lactate Dehydrogenase (LDH), lymphocytes, Urea, Alkaline phosphatase (AST), Neutrophils, and C-Reactive Protein (CRP). The levels of all the components increased significantly with the severity of the glioma, with maximum levels seen in glioblastoma (grade IV), followed by grade III and grade II, respectively.

Gliomas have significant clinical challenges due to their progression with heterogeneous nature and aggressive behavior. A liquid biopsy is a non-invasive approach that aids in setting up the status of the patient and figuring out the tumor grade; therefore, it may show diagnostic and prognostic utility. Additionally, our study provides evidence to prove the role of ABO blood group antigens in the development of glioma. However, future clinical research on liquid biopsy will improve the sensitivity and specificity of these tests and confirm their clinical usefulness to guide treatment approaches.

The objective is to analyze the prevalence of Alzheimer's disease in patients with and without a diagnosis of different autoimmune diseases and the possible association between both pathologies.

A multicenter, retrospective, cohort study was conducted to study the prevalence of Alzheimer's disease among patients diagnosed with various autoimmune diseases compared to the general population. Data from electronic medical records from the Castilla-La Mancha healthcare system were analyzed using Natural Language Processing through the Savana Manager® artificial intelligence clinical platform. A total of 1,028,356 patients were analyzed, including 28,920 individuals with Alzheimer's disease and 999,436 control patients.

Out of the 12 autoimmune diseases analyzed, 5 showed a significant association with Alzheimer's disease with p < 0.05. Myasthenia gravis had an increased prevalence of AD with OR 1.49 (95% CI 1.11-2), systemic lupus erythematosus with OR 2.42 (95% CI 2.02-2.88), rheumatoid arthritis with OR 1.38 (95% CI 1.24-1.54), polymyalgia rheumatica with OR 2.01 (95% CI 1.08-2.23), and pernicious anemia with OR 2.06 (95% CI 1.59-2.66). The remaining autoimmune diseases analyzed did not show a higher prevalence of Alzheimer's disease compared to the general population.

There may be an association between certain systemic autoimmune diseases and Alzheimer's disease. Further studies are needed to confirm our findings, establish causality, and explore the underlying mechanisms of this association.

Several studies investigated the risks of neurological conditions in patients with inflammatory bowel disease (IBD), with some variability in findings. We aimed to perform a systematic review and meta-analysis of available evidence to elucidate the association between IBD and the risks of common neurological disorders.

We conducted a literature search through Embase, PubMed, Scopus, and ProQuest databases from inception to June 30, 2023, to identify cohort studies assessing the risk of developing stroke, all-cause dementia, Parkinson's disease (PD), multiple sclerosis (MS), seizure/epilepsy, and peripheral neuropathy in adult IBD patients compared with non-IBD population. We combined hazard ratios (HRs) with 95% confidence intervals (CIs) to compute pooled estimates using a random-effects model.

In total, 22 cohort studies were included, of which 9 studies reported 7074 stroke events in 202 460 IBD patients, 5 studies reported 3783 all-cause dementia diagnoses in 109 602 IBD patients, 7 studies reported 932 PD diagnoses in 354 792 IBD patients, and 1 study reported 6 MS events in 35 581 IBD patients. We observed increased risks of incident stroke (pooled HR = 1.19; 95% CI, 1.06-1.31), all-cause dementia (pooled HR = 1.22; 95% CI, 1.05-1.38), PD (pooled HR = 1.39; 95% CI, 1.20-1.58), and MS (HR = 2.89; 95% CI, 1.02-8.42). No eligible studies were found on peripheral neuropathy and seizure/epilepsy.

Inflammatory bowel disease may be modestly associated with increased risks of stroke, all-cause dementia, and PD. Further longitudinal studies are warranted to investigate potential links with MS, seizure/epilepsy, and peripheral neuropathy, as well as their clinical significance.

Growing research suggests that food insecurity is associated with worse cognitive functioning; however, prospective studies are needed to examine food insecurity and dementia risk. Using longitudinal and nationally representative data, we examined the effects of food insecurity on dementia risk among older adults.

Data were from 3,232 adults (≥65 years) from the Panel Study of Income Dynamics. Food insecurity was assessed biennially using the U.S. Household Food Security Survey Module from 2015 to 2019. Probable dementia risk was assessed biennially using the Eight-Item Interview to Differentiate Aging and Dementia from 2017 to 2021. Inverse probability weighting and marginal structural models were used to account for the time-varying nature of food insecurity and sociodemographic and health confounders.

After accounting for baseline and time-varying sociodemographic and health covariates, there was a 2-fold higher association between food insecurity and probable dementia risk (odds ratio 2.11, 95% confidence interval: 1.12-3.98). The results were robust to expanding the exposure to include marginal food security and the outcome to include informant-reported memory loss. Furthermore, there was no evidence of heterogeneity in the association of food insecurity and probable dementia risk by sex, race, and ethnicity, or participation in the Supplemental Nutrition Assistance program.

Food insecurity is a modifiable social determinant of health. Interventions and policies are needed to reduce food insecurity and promote healthy aging for older adults.

Inflammation is a significant factor in adverse health outcomes, but the combined effects of diets with varying oxidation levels and exposure to volatile organic compounds (VOCs) on inflammation are not well understood. This study aimed to elucidate the effects of the recognized Dietary Oxidative Balance Score (DOBS) and five VOCs on the systemic immune-inflammation index (SII) and C-reactive protein (CRP).

This cross-sectional study included data from participants in three cycles (2003-2004, 2005-2006, 2009-2010) of the National Health and Nutrition Examination Survey (NHANES). We used Spearman correlation, logistic regression, and trend tests to explore the associations between DOBS, VOCs, SII, and CRP. Additionally, we conducted restricted cubic spline (RCS) analysis to assess dose-response relationships between exposure and effect. G-computation and stratified analyses were performed to further elucidate these associations.

We included 7033 eligible participants, with 48.8 % males and 51.2 % females. Spearman correlation revealed that DOBS was negatively correlated with SII and CRP, while the five VOCs were positively correlated with SII and CRP. Although fully adjusted logistic regression models did not yield statistically significant results, trend tests indicated a gradual decrease in SII and CRP with increasing DOBS, a finding validated by RCS analysis. G-computation results demonstrated that the combined effect of DOBS and VOCs on inflammation was positive, with DOBS exerting a negative effect and benzene, ethylbenzene, and 1,4-dichlorobenzene exerting positive effects. Stratified analysis showed that maintaining physical activity significantly influenced the effects of DOBS and VOCs on inflammation.

This study suggests that adjusting dietary structure and reducing daily exposure to VOCs can effectively reduce inflammation in the body.

Alzheimer's disease (AD) is a complex degenerative disease of the central nervous system, and elucidating its pathogenesis remains challenging. In this study, we used the inverse-variance weighted (IVW) model as the major analysis method to perform hypothesis-free Mendelian randomization (MR) analysis on the data from MRC IEU OpenGWAS (18,097 exposure traits and 16 AD outcome traits), and conducted sensitivity analysis with six models, to assess the robustness of the IVW results, to identify various classes of risk or protective factors for AD, early-onset AD, and late-onset AD. We generated 400,274 data entries in total, among which the major analysis method of the IVW model consists of 73,129 records with 4840 exposure traits, which fall into 10 categories: Disease, Medical laboratory science, Imaging, Anthropometric, Treatment, Molecular trait, Gut microbiota, Past history, Family history, and Lifestyle trait. More importantly, a freely accessed online platform called MRAD (https://gwasmrad.com/mrad/) has been developed using the Shiny package with MR analysis results. Additionally, novel potential AD therapeutic targets (CD33, TBCA, VPS29, GNAI3, PSME1) are identified, among which CD33 was positively associated with the main outcome traits of AD, as well as with both EOAD and LOAD. TBCA and VPS29 were negatively associated with the main outcome traits of AD, as well as with both EOAD and LOAD. GNAI3 and PSME1 were negatively associated with the main outcome traits of AD, as well as with LOAD, but had no significant causal association with EOAD. The findings of our research advance our understanding of the etiology of AD.

Hemodialysis patients (HDPs) exhibit extensive cardiovascular risk. The widely prescribed anti-platelet agent clopidogrel is metabolically activated by cytochrome enzymes, which may be impaired by uremia and chronic low-grade inflammation, typically present in HDPs. We conducted a prospective multicenter study to investigate the pharmacokinetics and pharmacodynamics of clopidogrel in HDPs and healthy volunteers (HVs).

We enrolled HDPs receiving long-term clopidogrel (75 mg) and pantoprazole treatment (40 mg). Healthy volunteers received a loading dose of 300 mg clopidogrel, followed by 75 mg once daily. Pantoprazole, a substrate and probe drug of CYP2C19, was administered intravenously (40 mg). Plasma concentrations were quantified by mass spectrometry. Pharmacokinetics were calculated, and a population pharmacokinetic model was developed. The primary endpoint was the maximum concentration of clopidogrel's active metabolite. Platelet aggregation was measured using adenosine diphosphate-induced whole-blood aggregometry.

Seventeen HDPs and 16 HVs were included. The maximum concentration of clopidogrel's active metabolite was significantly lower in HDPs compared to HVs (median [interquartile range] 12.2 [4.6-23.4] vs. 24.7 [17.8-36.5] ng/ml, P = 0.02). The maximum concentration ratio of clopidogrel's active metabolite to prodrug was 8.5-fold lower in HDPs, and an 82.7% reduced clopidogrel clearance, including clopidogrel's active metabolite formation, was found using population pharmacokinetic modeling. From previous studies, adenosine diphosphate-induced platelet aggregation at 120 minutes was significantly higher in HDPs than in HVs (median [interquartile range]: 26 U [14 U-43 U] vs. 12 U [11 U-18 U], P = 0.004. Pantoprazole terminal half-life was ∼1.7-fold higher in HDPs compared to HVs.

Our data demonstrate an altered metabolism of clopidogrel in HDPs in the context of lower CYP2C19 activity, with potential implications for other substances metabolized by this enzyme.

Sodium intake reduction is crucial for cardiovascular health, however, its lasting impact on dementia remains unclear.

We included 458,577 UK Biobank participants without dementia at baseline. We estimated 24-h urinary sodium (E24hUNa) using spot urinary parameters and obtained the incidence of all-cause dementia, Alzheimer's disease, and vascular dementia from multiple sources.

The mean E24hUNa was 3.0 g (1st-99th percentile: 1.5 g-5.1 g). Over a mean follow-up of 13.6 years, 7886 (1.7 %) participants developed all-cause dementia, including 3763 (0.8 %) Alzheimer's disease and 1851 (0.4 %) vascular dementia. In the restricted cubic spline model, we identify a potential cutoff of 3.13 g for E24hUNa, below which each 1 g decrease in E24hUNa was associated with 21 % (95 % confidence interval [CI] 1.11-1.34) higher all-cause dementia risk and 35 % (95 % CI 1.11-1.63) higher vascular dementia risk (P-value <0.001 for non-linearity). The hazard ratios were 1.15 (95 % CI, 1.07-1.24) for all-cause dementia and 1.21 (95 % CI 1.04-1.40) for vascular dementia among individuals with E24hUNa below 3.13 g compared to those with E24hUNa higher than 3.13 g.

One of the major limitations is the estimation of 24-h urinary sodium with spot urine samples.

An E24hUNa level below 3.13 g, equivalent to 3.37 g daily sodium intake, is associated with increased risks of all-cause and vascular dementia. This exploratory study suggests a potential lower limit below which the risk of dementia increases with a lower sodium level. Future studies are necessary to validate our findings.

Consistent evidence shows that magnesium (Mg) intake is associated with lower blood pressure (BP), and that lower BP is associated with improved cerebral health. However, recent findings indicate that the positive effect of dietary Mg intake on cerebral health is not mediated by a decrease in BP. As Mg's anti-inflammatory action is a plausible alternative mechanism, the objective of this study was to investigate the associations between Mg intake and inflammation to determine whether it mediates any neuroprotective effect.

Participants from the UK Biobank (n = 5775, aged 40-73 years, 54.7% female) were assessed for dietary magnesium using an online food questionnaire, brain and white matter lesion (WML) volumes were segmented with FreeSurfer software, and inflammation markers including high-sensitivity C-reactive protein (hs-CRP), leukocyte, erythrocyte count, and Glycoprotein acetylation (GlycA) were measured using specific laboratory techniques such as immunoturbidimetry, automated cell counting, and nuclear magnetic resonance. Hierarchical linear regression models were performed to investigate the association between dietary Mg, and inflammatory markers and between dietary Mg, brain and WMLs volumes. Mediation analysis was performed to test a possible mediation role of inflammation on the association between dietary Mg and brain and WMLs volumes.

Higher dietary Mg intake was associated with lower inflammation: hs-CRP level (- 0.0497%; 95% confidence interval [CI] - 0.0497%,  - 0.0199%) leukocytes count (- 0.0015%; 95%CI - 0.00151%,  - 0.0011%), and GlycA (- 0.0519%; 95%CI - 0.1298%,  - 0.0129%). Moreover, higher dietary Mg intake was associated with larger grey matter volume (0.010%; 95%CI 0.004%, 0.017%), white matter volume (0.012%; 95%CI 0.003,  0.022) and right hippocampal volume (0.002%; 95%CI 0.0007, -0.0025%). Lower hs-CRP levels mediated the positive association between higher dietary Mg intake and larger grey matter volume.

The anti-inflammatory effects of dietary Mg intake in the general population, appears to mediate its neuroprotective effect.

A growing body of literature examines the relationship between peripheral immune function and Alzheimer's Disease (AD) in human populations. Our living systematic review summarizes the characteristics and findings of these studies, appraises their quality, and formulates recommendations for future research.

We searched the electronic databases PubMed, PsycINFO, and Web of Science, and reviewed references of previous reviews and meta-analyses to identify human studies examining the relationship between any peripheral immune biomarkers and AD up to September 7th, 2023. We examined patterns of reported statistical associations (positive, negative, and null) between each biomarker and AD across studies. Evidence for each biomarker was categorized into four groups based on the proportion of studies reporting different associations: corroborating a positive association with AD, a negative association, a null association, and presenting contradictory findings. A modified Newcastle-Ottawa scale (NOS) was employed to assess the quality of the included studies.

In total, 286 studies were included in this review. The majority were cross-sectional (n = 245, 85.7%) and hospital-based (n = 248, 86.7%), examining relationships between 187 different peripheral immune biomarkers and AD. Cytokines were the most frequently studied group of peripheral immune biomarkers. Evidence supported a positive association with AD for six biomarkers, including IL-6, IL-1β, IFN-γ, ACT, IL-18, and IL-12, and a negative association for two biomarkers, including lymphocytes and IL-6R. Only a small proportion of included studies (n = 22, 7.7%) were deemed to be of high quality based on quality assessment.

Existing research on peripheral immune function and AD exhibits substantial methodological variations and limitations, with a notable lack of longitudinal, population-based studies investigating a broad range of biomarkers with prospective AD outcomes. The extent and manner in which peripheral immune function can contribute to AD pathophysiology remain open questions. Given the biomarkers that we identified to be associated with AD, we posit that targeting peripheral immune dysregulation may present a promising intervention point to reduce the burden of AD.

Inflammation and liver function are associated with cognitive decline and dementia. Little is known about the serum albumin-to-globulin ratio on cognitive function.

The objective of this study was to investigate the association between albumin-to-globulin ratio and cognitive function among the American older people.

The public data available on the US National Health and Nutrition Examination Survey (NHANES) from 2011 to 2014 was used for this cross-sectional study. Participants aged ≥60 years completed the cognitive function assessments, including word learning and recall modules from the Consortium to Establish a Registry for Alzheimer's Disease (CERAD), the animal fluency (AF) test, and the digit symbol substitution test (DSST). A composite cognition score was calculated to evaluate global cognition. The univariate and multivariate linear regression analysis, curve fitting, a threshold effect, along with a subgroup analysis and interaction tests were conducted.

Serum albumin-to-globulin ratio (per 0.1 unit) was positively associated DSST score (β = 0.36, 95% CI: 0.21, 0.51), AF score (β = 0.1, 95% CI: 0.04, 0.16) and global cognition score (β = 0.05, 95% CI: 0.02, 0.07), after being fully adjusted, while albumin-to-globulin ratio was not related to CERAD score (β = 0.05, 95% CI: -0.02, 0.12). A non-linear was observed in the dose-response relationship between albumin-to-globulin ratio and global cognition (P for non-linearity < 0.001). The subgroup analysis was overall stable, yet the interaction test was significant for age on global cognition (P for interaction = 0.036).

The findings of this cross-sectional study suggested a positive and non-linear association between albumin-to-globulin ratio and cognitive function in the American older people. Maintaining albumin-to-globulin ratio with an appropriate range may be one of the therapeutic strategies to limit the progression of cognitive decline for the older people.

Emerging evidence has shown that gut diseases can regulate the development and function of the immune, metabolic, and nervous systems through dynamic bidirectional communication on the brain-gut axis. However, the specific mechanism of intestinal diseases and vascular dementia (VD) remains unclear. We designed this study especially, to further clarify the connection between VD and inflammatory bowel disease (IBD) from bioinformatics analyses.

We downloaded Gene expression profiles for VD (GSE122063) and IBD (GSE47908, GSE179285) from the Gene Expression Omnibus (GEO) database. Then individual Gene Set Enrichment Analysis (GSEA) was used to confirm the connection between the two diseases respectively. The common differentially expressed genes (coDEGs) were identified, and the STRING database together with Cytoscape software were used to construct protein-protein interaction (PPI) network and core functional modules. We identified the hub genes by using the Cytohubba plugin. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis were applied to identify pathways of coDEGs and hub genes. Subsequently, receiver operating characteristic (ROC) analysis was used to identify the diagnostic ability of these hub genes, and a training dataset was used to verify the expression levels of the hub genes. An alternative single-sample gene set enrichment (ssGSEA) algorithm was used to analyze immune cell infiltration between coDEGs and immune cells. Finally, the correlation between hub genes and immune cells was analyzed.

We screened 167 coDEGs. The main articles of coDEGs enrichment analysis focused on immune function. 8 shared hub genes were identified, including PTPRC, ITGB2, CYBB, IL1B, TLR2, CASP1, IL10RA, and BTK. The functional categories of hub genes enrichment analysis were mainly involved in the regulation of immune function and neuroinflammatory response. Compared to the healthy controls, abnormal infiltration of immune cells was found in VD and IBD. We also found the correlation between 8 shared hub genes and immune cells.

This study suggests that IBD may be a new risk factor for VD. The 8 hub genes may predict the IBD complicated with VD. Immune-related coDEGS may be related to their association, which requires further research to prove.

Inflammatory bowel disease (IBD) refers to two chronic conditions of the digestive tract: ulcerative colitis (UC) and Crohn's disease (CD), representing a progressive inflammatory process that mainly occurs in the gut, with frequent extra-intestinal manifestations. Even if remission is periodically obtained for some patients, the histological activity and digestive symptoms may continue, maintaining a persistent systemic inflammation that could induce further extra-intestinal complications and contribute to the development of neurodegenerative disease. C-reactive protein (CRP) is an acute-phase reactant that is widely accepted as a dominant serum biomarker in IBD. CRP consequently activates the complement cascade, supports the release of pro-inflammatory cytokines, and the clearance of microbial pathogens. All these processes facilitate further processes, including atherosclerosis and hypercoagulability, alteration of the intestinal microbiota, and the increased permeability of the intestinal barrier for neurotoxic substances produced by gut microorganisms, due to the presence of a high level of lipopolysaccharides. For IBD, the connection between intestinal inflammation and central nervous system inflammation could be explained through the activity of the vagus nerve, a carrier of cytokines, CRP, and toxic materials to the brain, potentially inducing vascular lesions and damage of the glial vascular unit, with further risk for degeneration within the central nervous system. CRP is a key marker for IBD pathogenesis and is able to dissociate into its monomeric form, mCRP, on contact with activated cell and tissue components via the systemic circulation. We hypothesize that the chronic inflammatory process within IBD could initiate neuroinflammation and neurodegeneration, and therefore, further investigation of the significance of chronically raised plasma of CRP and mCRP in patients with IBD is warranted, as it may represent a critical predictive factor associated with a later neurodegenerative risk. Any future initiative aimed at pharmacologic modulation of CRP (e.g., blocking CRP-mCRP dissociation), could represent a new therapeutic approach protecting against intestinal inflammation and concomitantly reducing the risk of neuroinflammation, neurodegeneration, and cognitive decline.

To investigate the possible role of systemic inflammatory markers (interleukin; IL-6, C-reactive protein; CRP, and albumin levels) in the development of Alzheimer's dementia (AD) and also find their association with the severity of disease.

It was a cross-sectional study. Patients with Alzheimer's dementia (AD) and vascular dementia (VaD) from outpatient settings in tertiary care hospitals and non-demented controls (NDC) were recruited from the community. Individuals aged 50 years and older (n = 110) were included. Serum levels of IL-6, CRP, and albumin levels in patients with AD, VaD, and NDC were measured. The clinical Dementia Rating Scale was used for staging the severity of dementia. Serum levels of IL-6, CRP, and serum albumin were compared in study subjects and also analyzed with the severity of dementia in dementia subgroups.

Our main finding was that serum levels of IL-6 were significantly elevated in patients with AD and VaD (7.79 and 6.60) as compared to NDC (2.98) (P < 0.001). No significant difference in CRP or albumin levels was observed between the three groups. Serum IL-6 and CRP showed a positive correlation with the severity of AD, though the correlation was significant only for IL-6 (r = 0.777). The serum albumin levels showed a statistically significant negative correlation with the severity of AD (r > 0.3 but <0.5).

The study demonstrates a notable association between systemic inflammatory markers, particularly IL-6, and the severity of AD, indicating their potential role in its pathogenesis. These findings suggest that targeting these markers could offer new insights into therapeutic strategies for AD.

This study explored the dynamic functional connective (DFC) alterations in patients with rheumatoid arthritis (RA) and investigated the correlation between the neuropsychiatric symptoms, peripheral inflammation and DFC alterations.

Using resting-state functional MRI, we investigated the DFC based on spatial independent component analysis and sliding window method for 30 patients with RA and 30 healthy controls (HCs). The Spearman correlation was calculated between aberrant DFC alterations, Montreal Cognitive Assessment (MoCA), Hospital Anxiety and Depression Scale (HAD), C reactive protein (CRP) and erythrocyte sedimentation rate (ESR). Diagnostic efficacy of indicators was assessed using receiver operating characteristic analysis (ROC).

Three dynamic functional states were identified. Compared with HC, patients with RA showed reduced FC variabilities between sensorimotor network (SMN) and insula, SMN and orbitofrontal cortex, which were the crucial regions of sensory processing network. The above FC variabilities were correlated with the MoCA, HAD, CRP and ESR in patients with RA. Additionally, the CRP and ESR were negatively correlated to MoCA and positively related to HAD in patients with RA. The ROC analysis results showed that MoCA, HAD and FC variabilities of the sensory processing network could distinguish patients with RA from HC and also identify patients with RA with high ESR.

Our findings demonstrated that abnormal DFC patterns in sensory processing networks in patients with RA were closely associated with peripheral inflammation and neuropsychiatric symptoms. This indicates that the dynamic temporal characteristics of the brain functional network may be potential neuroimaging biomarkers for revealing the pathological mechanism of RA.

Parkinson's disease (PD), a widely recognized neurodegenerative disorder, is characterized by a spectrum of symptoms including motor fluctuations and dyskinesia. Neuroinflammation and dysregulation of adipokines are increasingly implicated in the progression of PD. This preliminary study investigated the levels of inflammatory biomarkers and adipokines, namely interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), C-reactive protein (CRP), visfatin, progranulin, and 25(OH)-vitamin D in 52 PD patients, divided equally between those with and without dyskinesia and 26 healthy controls. Significant differences in the levels of IL-6, TNF-α, visfatin, and progranulin were noted between the groups. Patients with dyskinesia exhibited notably higher IL-6 levels compared to controls, and TNF-α was significantly elevated in both PD patient groups relative to the control group. Additionally, visfatin levels were higher in PD patients without dyskinesia as opposed to those with dyskinesia, and progranulin levels were elevated in the non-dyskinetic PD group compared to controls. The findings highlight the potential role of the examined biomarkers in the pathophysiology of PD. Changes in levels of the tested inflammatory biomarkers and adipokines might be associated with Parkinson's disease and its symptoms such as dyskinesia.

Numerous observational studies have documented a correlation between inflammatory bowel disease (IBD) and an increased risk of dementia. However, the causality of their associations remains elusive.

To assess the causal relationship between IBD and the occurrence of all-cause dementia using the two-sample Mendelian randomization (MR) method.

Genetic variants extracted from the large genome-wide association study (GWAS) for IBD (the International IBD Genetics Consortium, n = 34652) were used to identify the causal link between IBD and dementia (FinnGen, n = 306102). The results of the study were validated via another IBD GWAS (United Kingdom Biobank, n = 463372). Moreover, MR egger intercept, MR pleiotropy residual sum and outlier, and Cochran's Q test were employed to evaluate pleiotropy and heterogeneity. Finally, multiple MR methods were performed to estimate the effects of genetically predicted IBD on dementia, with the inverse variance wei-ghted approach adopted as the primary analysis.

The results of the pleiotropy and heterogeneity tests revealed an absence of significant pleiotropic effects or heterogeneity across all genetic variants in outcome GWAS. No evidence of a causal effect between IBD and the risk of dementia was identified in the inverse variance weighted [odds ratio (OR) = 0.980, 95%CI : 0.942-1.020, P value = 0.325], weighted median (OR = 0.964, 95%CI : 0.914-1.017, P value = 0.180), and MR-Egger (OR = 0.963, 95%CI : 0.867-1.070, P value = 0.492) approaches. Consistent results were observed in validation analyses. Reverse MR analysis also showed no effect of dementia on the development of IBD. Furthermore, MR analysis suggested that IBD and its subtypes did not causally affect all-cause dementia and its four subtypes, including dementia in Alzheimer's disease, vascular dementia, dementia in other diseases classified elsewhere, and unspecified dementia.

Taken together, our MR study signaled that IBD and its subentities were not genetically associated with all-cause dementia or its subtypes. Further large prospective studies are warranted to elucidate the impact of intestinal inflammation on the development of dementia.

Neurodegenerative disease (ND) incidence has recently increased due to improved life expectancy. Alzheimer's (AD) or Parkinson's disease (PD) are the most prevalent NDs. Both diseases are poly genetic, multifactorial and heterogenous. Preventive medicine, a healthy diet, exercise, and controlling comorbidities may delay the onset. After the diseases are diagnosed, therapy is needed to slow progression. Recent studies show that local, peripheral and age-related inflammation accelerates NDs' onset and progression. Patients with autoimmune disorders like inflammatory bowel disease (IBD) could be at higher risk of developing AD or PD. However, no increase in ND incidence has been reported if the patients are adequately diagnosed and treated. Autoantibodies against abnormal tau, β amyloid and α- synuclein have been encountered in AD and PD and may be protective. This discovery led to the proposal of immune-based therapies for AD and PD involving monoclonal antibodies, immunization/ vaccines, pro-inflammatory cytokine inhibition and anti-inflammatory cytokine addition. All the different approaches have been analysed here. Future perspectives on new therapeutic strategies for both disorders are concisely examined.

Numerous studies have investigated the correlation between malondialdehyde (MDA) and cognitive decline. However, limited research has explored the interplay between superoxide dismutase (SOD), C-reactive protein (CRP), and MDA.

This study aims to scrutinize the association between MDA and cognitive function in older adults, while also elucidating the roles of SOD and CRP within this relationship.

Utilizing data from the Chinese Longitudinal Healthy Longevity Survey (CLHLS) spanning 2008-2009, 2011-2012, and 2014, this study included 2,696 eligible subjects. Cognitive function was evaluated using the Chinese version of the Mini-Mental State Examination (MMSE). Linear mixed-effects models were employed to examine the links between MDA, SOD, CRP, and their interactions with cognitive function.

Elevated serum levels of MDA and CRP, as well as decreased serum SOD levels, were related to decreased cognitive function (β= -0.220 and -0.346, 95% CI: -0.399, -0.041 and -0.526, -0.167 for MDA and CRP; β= 0.384, 95% CI: 0.204, 0.564 for SOD). Notably, a significant interaction between MDA and SOD was detected (p = 0.001). An increase per standard deviation in serum MDA levels was significantly associated with a 0.347-point lower MMSE score only in participants with normal cognitive function and high SOD levels (β= -0.347, 95% CI: -0.497, -0.197; p < 0.001).

Elevated serum MDA levels in the normal population with high SOD levels suggested diminished cognitive performance. Combining MDA with SOD could be pivotal in identifying older adults at risk of cognitive decline in clinical settings.

Circulating C-reactive protein (pCRP) concentrations rise dramatically during both acute (e.g., following stroke) or chronic infection and disease (e.g., autoimmune conditions such as lupus), providing complement fixation through C1q protein binding. It is now known, that on exposure to the membranes of activated immune cells (and microvesicles and platelets), or damaged/dysfunctional tissue, it undergoes lysophosphocholine (LPC)-phospholipase-C-dependent dissociation to the monomeric form (mCRP), concomitantly becoming biologically active. We review histological, immunohistochemical, and morphological/topological studies of post-mortem brain tissue from individuals with neuroinflammatory disease, showing that mCRP becomes stably distributed within the parenchyma, and resident in the arterial intima and lumen, being "released" from damaged, hemorrhagic vessels into the extracellular matrix. The possible de novo synthesis via neurons, endothelial cells, and glia is also considered. In vitro, in vivo, and human tissue co-localization analyses have linked mCRP to neurovascular dysfunction, vascular activation resulting in increased permeability, and leakage, compromise of blood brain barrier function, buildup of toxic proteins including tau and beta amyloid (Aβ), association with and capacity to "manufacture" Aβ-mCRP-hybrid plaques, and, greater susceptibility to neurodegeneration and dementia. Recently, several studies linked chronic CRP/mCRP systemic expression in autoimmune disease with increased risk of dementia and the mechanisms through which this occurs are investigated here. The neurovascular unit mediates correct intramural periarterial drainage, evidence is provided here that suggests a critical impact of mCRP on neurovascular elements that could suggest its participation in the earliest stages of dysfunction and conclude that further investigation is warranted. We discuss future therapeutic options aimed at inhibiting the pCRP-LPC mediated dissociation associated with brain pathology, for example, compound 1,6-bis-PC, injected intravenously, prevented mCRP deposition and associated damage, after temporary left anterior descending artery ligation and myocardial infarction in a rat model.

Breast cancer is the most commonly diagnostic cancer in women worldwide. The main treatment for these patients is surgery. However, there is a high incidence of surgical site infection (SSI) in breast cancer patients. The aim of this study was to identify effective infection-related diagnostic markers for timely diagnosis and treatment of SSI.

This retrospective study included 263 breast cancer patients who were treated between July 2018 and March 2023 at the Shandong Cancer Hospital and Institute. We analyzed differences between the SSI group and control group and differences before and during infection in the SSI group. Finally, we tested the distribution of pathogenic microorganisms and their susceptibility to antibiotics.

Compared with preoperative inflammatory indicators, white blood cells (WBC), neutrophils (NEU), absolute neutrophil count to the absolute lymphocyte count (NLR), D2 polymers (D-Dimer) and fibrinogen (FIB) were significantly increased, while lymphocytes (LYM), albumin (ALB) and prealbumin (PA) were significantly decreased in the SSI group. Compared with uninfected patients, WBC, NEU, NLR and FIB were significantly increased, ALB and PA were significantly decreased in SSI patients, while LYM and D-Dimer did not differ significantly. The distribution of infection bacteria in SSI patients showed that the proportion of patients with Staphylococcus aureus infection was as high as 70.41%; of those patients, 19.33% had methicillin-resistant Staphylococcus aureus (MRSA) infection. The area under the curves (AUCs) of the receiver operating curves (ROCs) for WBC, NEU, NLR, FIB, ALB and PA were 0.807, 0.811, 0.730, 0.705, 0.663 and 0.796, respectively. The AUCs for other inflammatory indicators were not statistically significant. There was no significant difference in antibiotic resistance for Staphylococcus aureus when compared to that of gram-positive bacteria. The resistance of gram-positive bacteria to ceftriaxone (CRO), cefoxitin (FOX), chloramphenicol (CHL), minocycline (MNO) and tetracycline (TCY) was lower than that of gram-negative bacteria, while the resistance to gentamicin (GEN) was higher.

This study demonstrated that WBC, NEU, NLR, FIB and PA have good predictive value for identifying patients at risk of SSI. The cut-off values of inflammatory indicators can be helpful in the prevention and diagnosis of SSI.

Postoperative delirium (POD) is a common complication in operative patients. Neuroinflammation has been reported to be a potential mechanism associated with the development of POD. Identifying available inflammatory markers such as C-reactive protein (CRP) would aid clinicians in early detection of POD. Previous studies have demonstrated that CRP may be a promising predictive marker for POD. Thus, this study aimed to explore the association between CRP and POD among those elderly colorectal cancer (CRC) patients.

643 patients with CRC were included in this study. CRP levels were measured before operation and on postoperative day 1. The univariate and multivariate regression analyses were used to identify risk factors for POD.

Of 643 patients with CRC, 112 cases (17.4%) had POD. CRC patients with POD showed older age, higher CRP level on postoperative day 1, and higher percentage of smoking, diabetes mellitus, and chronic obstructive pulmonary disease (COPD) than CRC patients without POD. Preoperative CRP level was not associated with the POD. Univariate and multivariate regression analyses showed that older age (> 70 years), diabetes mellitus, COPD, and higher CRP level on postoperative day 1 (> 48 mg/L) were risk factors for POD in CRC patients.

Postoperative CRP level is an independent indicator for POD among CRC patients, suggesting the predictive role of postoperative CRP levels for POD in elderly CRC patients undergoing surgery.

Alzheimer's disease (AD) and/or dementia is a prevalent neurocognitive disorder primarily affecting individuals over the age of 65. Identifying specific causes of AD and/or dementia can be challenging, with emerging evidence suggesting a potential association with autoimmune inflammatory conditions such as rheumatoid arthritis (RA). This study aimed to assess the prevalence rate of AD and/or dementia among Medicare beneficiaries reporting an autoimmune disorder. Additionally, this study sought to identify the comparative prevalence of AD and/or dementia in patients with an autoimmune disorder who were using disease-modifying antirheumatic drugs (DMARDs) compared to those not using DMARDs.

Cross-sectional secondary data analyses were conducted on Medicare Current Beneficiary Survey (MCBS) data from 2017 and 2018. The MCBS data consists of a nationally representative sample of the Medicare population, a population that is largely 65 and older, and provides de-identified patient information. Patients from this dataset with a self-reported autoimmune disorder were included in the analyses. Descriptive analyses were conducted on demographic variables, chronic conditions, and medication use. The prevalence of AD and/or dementia was compared between patients with and without an autoimmune disorder. A backward stepwise selection regression was used to identify the risk factors associated with the prevalence of AD and/or dementia.

The study included 18,929 Medicare beneficiaries, with 4,405 identified as having one autoimmune disorder. The prevalence of AD and/or dementia was significantly higher in patients with an autoimmune disorder. The multivariate regression showed that RA was significantly associated with a higher risk of AD and/or dementia. Other demographic factors, including advanced age, African-American or Hispanic ethnicity, low body mass index, and chronic conditions of ischemic heart disease, history of myocardial infarction, history of stroke, depression, mental health disorder(s), and traumatic brain injury also showed statistically significant associations with AD and/or dementia. Patients using DMARDs demonstrated a reduced likelihood of having AD and/or dementia, compared to patients not using DMARDs.

This study provides evidence of an association between RA and increased risk of AD and/or dementia. The findings suggest that DMARD use may have a protective effect against the development of AD and/or dementia in patients with an autoimmune disorder.