BACKGROUND:Psychosocial adaptation is a key indicator for chronic disease rehabilitation. Many instruments have been proposed to evaluate psychosocial adaptation in individuals with chronic disease, but their measurement properties are unknown. OBJECTIVES:This systematic review aims to identify and critically assess the measurement properties of all existing instruments intended for measuring psychosocial adaptation in adults with chronic disease. METHODS:A systematic search was conducted in PubMed, Embase, CINAHL, PsycINFO, Chinese databases, including China National Knowledge Infrastructure (CNKI), and Wan Fang from their inception to July 10, 2025. The search followed the COSMIN guideline for systematic reviews of patient-reported outcome measures. RESULTS:Out of the 8,399 retrieved studies, only 24 studies that concerned 13 instruments were eventually included. Five instruments showed high-quality evidence from one measurement property, and two instruments were rated high-quality evidence from three and four measurement properties, respectively. There was no sufficient evidence for which instruments identified for assessing psychosocial adaptation in adults with chronic disease appear to be generally superior to the others. Therefore, further studies are recommended to validate the measurement properties of existing psychosocial adaptation instruments for adults with chronic disease. DISCUSSION:A total of 13 instruments were identified. However, current evidence for selecting instruments suitable for assessing psychosocial adaptation in adults with chronic disease was insufficient.

Hydroxycarboxylic acid receptor 1 (HCAR1) is a class A G protein-coupled receptor (GPCR) that is activated by the endogenous metabolite l-lactate and that plays an important role in various metabolic and inflammatory disorders. HCAR1 uses distinct ligand recognition and self-activation mechanisms to mediate specific pathophysiological functions through Gαi/o and β-arrestin signaling pathways. To support effective drug development targeting HCAR1, we investigated ligand recognition and activation mechanisms through cryo-electron microscopy (cryo-EM) structures of the HCAR1-Gαi1 complex in the apo state or with l-lactate or with the synthetic agonist CHBA. Compared with other HCARs, HCAR1 has a more compact binding pocket, which is stabilized by three unique disulfide bonds. l-lactate exhibited a flexible binding mode and relatively weak intermolecular interactions, thus requiring millimolar concentrations for receptor activation. In contrast, the binding of CHBA was more stable because of its chlorinated benzene ring, thus resulting in improved agonist potency. Structural comparisons with HCAR2 identified critical residues that restrict the size of the binding pocket of HCAR1 and influence ligand selectivity. Self-activation of HCAR1 is driven by conformational rearrangements within extracellular loop 2, with Phe168ECL2 playing a pivotal role as the key agonist. Together, these results clarify the mechanisms underlying HCAR1 activation, self-activation, and ligand selectivity, providing a structural framework for the design of high-affinity, selective agonists and inverse agonists with minimized off-target effects.

Emerging evidence suggests that nucleotide-binding oligomerization domain-like receptor protein 3 (NLRP3) inflammasome activation contributes to diabetic cognitive impairment (DCI), making its inhibition a potential therapeutic strategy for DCI. Akkermansia muciniphila (A. muciniphila) has shown benefits in metabolic diseases, neurodegenerative disorders, and neuroinflammation. However, its effect on NLRP3 inflammasome activation in the hippocampus of DCI mice remains unclear. This study aims to explore the effects and underlying mechanisms of A. muciniphila treatment in DCI mice. Herein, we demonstrated that the relative abundance of A. muciniphila was significantly decreased in patients with type 2 diabetes mellitus with normal cognition and in DCI patients compared to healthy participants. Oral administration of either live or pasteurized A. muciniphila significantly ameliorated the symptoms of cognitive impairment induced by a high-fat diet, as evidenced by reduced impairments in learning and memory, decreased neuronal loss, ameliorated impairments in synaptic plasticity, and increased expression of postsynaptic density protein-95 and synaptophysin proteins. Furthermore, A. muciniphila alleviated gut microbiota dysbiosis and neuroinflammation in DCI mice and simultaneously inhibited the activation of the NLRP3 inflammasome. However, the beneficial effects were abolished when A. muciniphila intervention was applied to NLRP3 knockout mice. These results emphasize the potent efficacy of A. muciniphila in alleviating DCI by inhibiting the activation of the NLRP3 inflammasome and ameliorating hippocampal synaptic defects. This study provides insights into the underlying mechanisms and presents a novel avenue for probiotic-based treatment of DCI.

Diabetes-related cognitive impairment (DCI) is a severe complication of type 2 diabetes mellitus (T2DM), with limited understanding of its molecular mechanisms hindering effective therapeutic development. This study identified SERPINA3 as a potential therapeutic target for DCI through integrated machine learning and molecular docking analyses. Transcriptomic data from cortical neuronal samples of T2DM patients were analysed using support vector machine recursive feature elimination (SVM-RFE) and least absolute shrinkage and selection operator (LASSO) regression, revealing SERPINA3 as a significantly upregulated gene in DCI. Experimental validation via Western blot confirmed elevated SERPINA3 protein levels in DCI patient plasma. Molecular docking demonstrated the stable binding of sulfonylurea hypoglycaemic agents, such as gliclazide and glimepiride, to SERPINA3, with binding energies of -6.8 and -6.6 kcal/mol, respectively. These findings suggest that SERPINA3 plays a pivotal role in DCI pathogenesis and that sulfonylurea drugs may exert neuroprotective effects through SERPINA3-mediated pathways. This study provides novel insights into the molecular mechanisms of DCI and highlights the potential of SERPINA3-targeted therapies for early intervention and treatment. Further research is warranted to validate these findings in larger cohorts and explore their clinical applicability.

This study investigates the causal relationship between coffee consumption patterns, propionic acid-producing gut microbiota, and glycated haemoglobin (HbA1c) levels using Mendelian randomisation (MR). Genome-wide association study datasets from the UK Biobank and MiBioGen consortium were analysed, identifying a significant mediating pathway: unsweetened filter coffee consumption promotes Veillonella abundance, which in turn reduces HbA1c levels. The inverse variance weighted method served as the primary analytical approach, supported by sensitivity analyses to ensure robustness. These findings highlight the potential of unsweetened filter coffee as a dietary intervention to improve glycaemic control by modulating gut microbiota. This research provides novel insights into the coffee-intestinal microbiota-metabolism axis and offers practical guidance for diabetes management, emphasising the importance of coffee preparation methods and dietary habits in harnessing its therapeutic potential.

Epidemiological studies suggest a link between type 2 diabetes mellitus (T2DM) and Alzheimer's disease (AD), possibly due to gut microbiota dysbiosis, although the exact mechanisms are unclear. This narrative review uniquely addresses how gut microbiota‐derived metabolites mediate overlapping pathologies of insulin resistance, neuroinflammation, and amyloidogenesis in T2DM and AD, proposing a framework for dual therapeutic targeting. This narrative review provides an in‐depth examination of the roles and mechanisms of gut microbiota and their metabolites in the context of T2DM and AD. This study indicates that gut microbiota dysbiosis significantly impacts the pathogenesis and progression of both diseases by modulating metabolic pathways, immune functions, and inflammatory responses. Key bacteria, such as Akkermansia muciniphila (which releases outer membrane vesicles), Lactobacillus , and Bifidobacterium , as well as their metabolites like short‐chain fatty acids (SCFAs), bile acids (BAs), lipopolysaccharide (LPS), vitamins, and Trimethylamine N‐oxide (TMAO) regulate T2DM and AD through complex mechanisms. Multiple signaling pathways, including G‐protein coupled receptor 41/43 (GPR41/43), phosphoinositide 3‐kinase (PI3K)/protein kinase B (Akt), Toll‐like receptor 4 (TLR4)/nuclear factor kappa‐light‐chain‐enhancer of activated B cells (NF‐κB), and endoplasmic reticulum (ER) stress‐mediated pathways, are also involved. These findings offer insights into the pathogenesis and potential targeted therapies for T2DM and AD.

Objectives: Alzheimer’s disease (AD) is a devastating neurodegenerative disorder with a complex aetiology. The aims of this study were to investigate the relationship between vitamin B supplementation and AD risk and to explore the potential mediating effect of the gut microbiota in this relationship. Methods: We employed a Mendelian randomisation analysis to examine the association between different vitamin B supplementation modalities (vitamin B6, folic acid, B12, and vitamin B complex tablets) and AD risk. Univariate Mendelian randomisation with inverse-variance weighting was used. Additionally, mediation analyses were conducted to identify the potential mediating effects of 119 known bacterial genera. Results: The univariate Mendelian randomisation analyses showed no significant direct associations between individual vitamin B supplements or vitamin B complex tablets and AD risk. However, several gut bacterial genera were significantly associated with AD risk. Lachnospiraceae (NK4A136 group), Paraprevotella, Slackia, and Bifidobacterium were associated with reduced AD risk, while Defluviitaleaceae (UCG011), Desulfovibrio, Eubacterium ventriosum group, and Ruminococcaceae UCG-003 were associated with increased AD risk. The mediation analysis revealed that Lachnospiraceae (NK4A136 group), Defluviitaleaceae (UCG011), and Bifidobacterium fully mediated the causal relationships between vitamin B12, B6, and B complex supplementation, respectively, and AD risk. Conclusions: This study provides evidence suggesting that certain gut microbiota genera are significantly associated with AD risk and may mediate the relationship between vitamin B supplementation and AD risk. These findings offer new insights into the variable effectiveness of B vitamins in treating neurodegenerative diseases and suggest potential new strategies for AD treatment and prevention.

Objectives: To provide a basis for further research on the molecular mechanisms underlying type 2 diabetes-associated mild cognitive impairment (DCI) using two bioinformatics methods to screen key genes involved in the progression of mild cognitive impairment (MCI) and type 2 diabetes. Methods: RNA sequencing data of MCI and normal cognition groups, as well as expression profile and sample information data of clinical characteristic data of GSE63060, which contains 160 MCI samples and 104 normal samples, were downloaded from the GEO database. Hub genes were identified using weighted gene co-expression network analysis (WGCNA). Protein–protein interaction (PPI) analysis, combined with least absolute shrinkage and selection operator (LASSO) and receiver operating characteristic (ROC) curve analyses, was used to verify the genes. Moreover, RNA sequencing and clinical characteristic data for GSE166502 of 13 type 2 diabetes samples and 13 normal controls were downloaded from the GEO database, and the correlation between the screened genes and type 2 diabetes was verified by difference and ROC curve analyses. In addition, we collected clinical biopsies to validate the results. Results: Based on WGCNA, 10 modules were integrated, and six were correlated with MCI. Six hub genes associated with MCI (TOMM7, SNRPG, COX7C, UQCRQ, RPL31, and RPS24) were identified using the LASSO algorithm. The ROC curve was screened by integrating the GEO database, and revealed COX7C, SNRPG, TOMM7, and RPS24 as key genes in the progression of type 2 diabetes. Conclusions: COX7C, SNRPG, TOMM7, and RPS24 are involved in MCI and type 2 diabetes progression. Therefore, the molecular mechanisms of these four genes in the development of type 2 diabetes-associated MCI should be studied.

Diabetes mellitus type 2 might cause mild cognitive impairment in its advanced stages,potentially progressing to dementia.Diabetic cognitive impairment(DCI)stands as a chronic complication of diabetes mellitus,with its underlying pathogenesis still remaining elusive.Research has revealed that gut microbiota dysbiosis influenced the central nervous system through the"microbiota-gut-brain axis",thereby contributing to the progression of cognitive impairment.Therefore,the regulation of gut microbiota emerges as a promising approach to the prevention and treatment of DCI.This article comprehensively reviews the mechanisms through which gut microbiota influences DCI.Furthermore,it delves into experimental studies exploring targeted therapies for gut microbiota,including probiotics,fecal microbiota transplantation,dietary and nutrient interventions,as well as traditional Chinese medicine.These studies not only address diabetes-related cognitive impairment but also consider aspects such as glycolipid metabolism and inflammation.The insights gleaned from these studies provide valuable guidance for the clinical application of gut microbiota-targeted intervention in DCI.

The established role of disturbances in the microbiota-gut-brain axis in the development of diabetic cognitive impairment (DCI) has long been recognized. It has shown the potential of Akkermansia muciniphila (A. muciniphila) in improving metabolic disorders and exerting anti-inflammatory effects. However, there remains a lack of comprehensive understanding regarding the specific effects and mechanisms underlying the treatment of DCI with A. muciniphila. This study aimed to evaluate the potential of A. muciniphila in alleviating DCI in db/db mice. Eleven-week-old db/db mice were administered either live or pasteurized A. muciniphila (5 x 109 CFU/200 mu L) for a duration of eight weeks. Administering live A. muciniphila significantly ameliorated cognitive impairments, improved the synaptic ultrastructure, and inhibited hippocampal neuron loss in the CA1 and CA3 subregions in db/db mice. Both live and pasteurized A. muciniphila effectively mitigated neuroinflammation. Moreover, live A. muciniphila increased the relative abundance of Lactococcus and Staphylococcus, whereas pasteurized A. muciniphila increased the relative abundance of Lactobacillus, Prevotellaceae_UCG_001, and Alistipes. Supplementation of A. muciniphila also induced alterations in serum and brain metabolites, with a particular enrichment observed in tryptophan metabolism, glyoxylate and dicarboxylate metabolism, nitrogen metabolism, and pentose and glucuronate interconversions. Correlation analysis further demonstrated a direct and substantial correlation between the altered gut microbiota and the metabolites in the serum and brain tissue. In conclusion, the results indicate that live A. muciniphila demonstrated greater efficacy compared to pasteurized A. muciniphila. The observed protective effects of A. muciniphila against DCI are likely mediated through the neuroinflammation and microbiota-metabolites-brain axis.

Abstract Background: Type 2 diabetes mellitus (T2DM), a growing global chronic disease, can increase the risk of cognitive impairment. The microbiota-gut-brain axis has a crucial role in the development of neurological pathologies. Therefore, it is necessary to examine host-gut microbiota metabolites associated with diabetic cognitive impairment (DCI) progression. Objective: This study aimed to describe metabolic signatures, identify potential biomarkers in the progression from T2DM to DCI, and analyze the correlation between the potential biomarkers and clinical characteristics. Methods: A cross-sectional study involving 8 patients with T2DM and 8 with DCI was carried out between May 2018 and May 2020. The characteristic clinical data of the patients, such as demographics, hematological parameters, Mini-Mental State Examination, and Montreal Cognitive Assessment, were collected. Metabolomics profiling measured the host-gut microbiota metabolites in the serum. The potential biomarkers were found by getting intersection of the differential host-gut microbiota metabolites from multidimensional statistics (Orthogonal Partial Least Squares-Discriminant Analysis and permutation plot) and univariate statistics (independent-sample t test and Mann-Whitney U test). In addition, we examined the relationship between potential biomarkers and characteristic clinical data using the Spearman correlation coefficient test. Results: A total of 22 potential biomarkers were identified in the T2DM and DCI groups, including 15 upregulated potential biomarkers (such as gluconolactone, 4-hydroxybenzoic acid, and 3-hydroxyphenylacetic acid) and 7 downregulated potential biomarkers (such as benzoic acid, oxoglutaric acid, and rhamnose) in DCI group. Most of the potential biomarkers were associated with clinical characteristics, such as Mini-Mental State Examination, Montreal Cognitive Assessment, and glycated hemoglobin A1c. Conclusion: This study showed that metabolic signatures in the serum were associated with DCI development and clinical severity, providing new ideas for extensive screening and targeted treatment.

The purpose of the study was to investigate health-related quality of life (HRQOL) and its associated factors among elderly individuals with dyslipidemia in rural Northern China. A cross-sectional study was conducted on 457 elderly individuals. The EQ-5D-5L questionnaire was used to assess HRQOL. Sociodemographic, anthropometric, lifestyle and health information was collected using a structured and standardized questionnaire. The Tobit regression model and multiple linear regression analysis were used to assess factors associated with HRQOL parameters including utility index and visual analogue score (EQ-VAS). The mean age of the participating individuals was 68.04 ± 5.98 years. The median utility index and EQ-VAS scores were 0.942 (P25-P75: 0.876–1.000) and 80 (P25-P75: 70–90), respectively. Pain/discomfort was the most frequently reported complaint among the five health dimensions (50.5

Background : The importance of the gut microbiota in primary Sjogren’s syndrome is gaining significant recognition. This systematic review summarized the previous findings on the discrepancies in gut microbiota between patients with primary Sjogren’s syndrome and healthy controls. Methods : From the establishment of the database until September 1, 2023, we conducted searches using electronic databases. We were interested in identifying specific bacterial changes between primary Sjogren’s syndrome and healthy controls as our primary outcomes. Secondary outcomes included exploring the relationship between gut microbiota and clinical parameters. To assess the quality of the included studies, we used the Newcastle-Ottawa scale. Results : A total of 9 articles were included in the analysis, comprising 504 case groups and 1313 control groups. According to two or more of the included studies, it was found that the gut microbiota of primary Sjogren’s syndrome patients was characterized by decreased butyrate-producing bacteria and increased pro-inflammatory microorganisms, as well as significantly lower levels of Actinobacteria, Firmicutes, Fusobacteria, and Proteobacteria. Furthermore, the Firmicutes/Bacteroidetes ratio was lower in patients with primary Sjogren’s syndrome than in controls. Finally, it was found that Roseburia has been shown to have a negative correlation with disease activity, as well as a negative correlation with IL-12 and IL-6. Conclusions : Patients with primary Sjogren’s syndrome exhibited reduced diversity in their gut microbiota and decreased abundance of short-chain fatty acid producers, which may offer potential therapeutic targets for future interventions. Trial registration : CRD42023421915.

This study aimed to quantitatively estimate the correlation between systemic inflammation with cognitive function, as well as glycemic and lipid profiles in patients with type 2 diabetes mellitus (T2DM). The PubMed, Web of Science, EMBASE, SCOPUS, CNKI, Wanfang, VIP, and CBM databases were searched from its inception until June 2023 (PROSPERO registration: CRD42022356889). We analyzed data extracted from observational studies to quantify the correlations (r) as the pooled effect size and further performed subgroup analyses and sensitivity analyses. A total of 32 studies involving 7,483 patients with T2DM were included. The findings revealed a significant moderate negative correlation between interleukin-6 (IL-6), tumor necrosis factor-α (TNF-α), and C-reactive protein (CRP) levels with Montreal Cognitive Assessment scores. TNF-α levels also had moderate negative correlation with Mini-Mental State Examination scores. For glycemic and lipid profiles, there was a significant moderate positive correlation between CRP and TNF-α levels and glycated hemoglobin (HbA1c), and TNF-α levels were also found to be lowly positively correlated with fasting blood glucose (FBG). CRP levels were found to have a low positive correlation with total cholesterol (TC), and IL-6 levels were found to be lowly positively correlated with triglycerides. The results indicate that elevated levels of IL-6, CRP, and TNF-α are significantly associated with cognitive impairment in patients with T2DM and may serve as inflammatory markers for T2DM with mild cognitive impairment. The CRP and TNF-α levels were more strongly correlated with HbA1c than with FBG and TC. Further research is needed to determine the clinical value of these inflammatory biomarkers and to investigate potential causal mechanisms underlying this association.

Short-chain fatty acids (SCFAs), the main metabolites of gut microbiota, have been associated with lower blood glucose and lipid levels in diabetic mice. However, a comprehensive summary and comparison of the effects of different SCFA interventions on blood glucose and lipid levels in diabetic mice is currently unavailable. This study aims to compare and rank the effects of different types of SCFAs on blood glucose and lipid levels by collecting relevant animal research. A systematic search through PubMed, Embase, Cochrane Library, and Web of Science database was conducted to identify relevant studies from inception to March 17, 2023. Both pairwise meta-analysis and Bayesian network meta-analysis were used for statistical analyses. In total, 18 relevant studies involving 5 interventions were included after screening 3793 citations and 53 full-text articles. Notably, butyrate therapy (mean difference [MD] = -4.52, 95% confidence interval [-6.29, -2.75]), acetate therapy (MD = -3.12, 95% confidence interval [-5.79, -0.46]), and propionate therapy (MD = -2.96, 95% confidence interval [-5.66, -0.26]) significantly reduced the fasting blood glucose levels compared to the control group; butyrate therapy was probably the most effective intervention, with a surface under the cumulative ranking curve (SUCRA) value of 85.5%. Additionally, acetate plus propionate therapy was probably the most effective intervention for reducing total cholesterol (SUCRA = 85.8%) or triglyceride levels (SUCRA = 88.1%). These findings underscore the potential therapeutic implications of SCFAs for addressing metabolic disorders, particularly in type 2 diabetes mellitus.

The available evidence regarding the association between adherence to the Alternate Mediterranean Diet (AMED) and Dietary Approaches to Stop Hypertension (DASH) dietary patterns and cognitive performance exhibits inconsistency, and its applicability within the Asian population remains uncertain. The association between adherence to the Chinese Food Pagoda (CHFP) and cognitive function is also unknown. In this study, we aimed to assess the association between adherence to the AMED, DASH, and CHFP different dietary patterns and cognitive function. The study included 3353 Chinese adults aged 55 years and over from the China Health and Nutrition Survey (CHNS) in 2006. A 24 h dietary recall over three consecutive days was used to collect dietary information. Dietary patterns included AMED, DASH, and CHFP. A subset of items from the Telephone Interview for Cognitive Status-Modified was used for cognitive screening. Poor cognitive performance was defined as a global cognitive function score < 7. Binary logistic regression was used to estimate the association between adherence to the three different dietary patterns and cognitive function. Binary logistic regression analysis showed that there is a negative association between higher adherence to the AMED, DASH, and CHFP and poorer cognitive performance (AMED: OR = 0.594, 95% CI = 0.458–0.771, p < 0.001; DASH: OR = 0.652, 95% CI = 0.504–0.843, p = 0.001; CHFP: OR = 0.599, 95% CI = 0.417–0.861, p = 0.006). There was a significant interaction between each of the three dietary patterns and residential regions (AMED: p for interaction = 0.045; DASH: p for interaction = 0.003; CHFP: p for interaction < 0.001). Higher adherence to the AMED, DASH, and CHFP dietary patterns was inversely associated with poor cognition in Chinese middle-aged and elderly adults, particularly among urban residents.

BackgroundIn nursing homes, elder neglect has come to the forefront. Currently, few studies have examined the impact of personal and organizational factors of geriatric nursing assistants on elder neglect. From the perspective of geriatric nursing assistants, this study aims to explore the current situation and influencing factors of elder neglect in Chinese nursing homes.MethodsA convenience sampling method was used to recruit 412 geriatric nursing assistants from 50 nursing homes in China. Participants were surveyed using a demographic questionnaire, the Elder Neglect Scale for Geriatric Nursing Assistants, the General Self-Efficacy Scale (GSES), and the Proactive Personality Scale (PPS). Spearman correlation analysis and multiple linear regression were used to analyze the factors influencing elder neglect.ResultsGeriatric nursing assistants scored a median of 74 out of 85 on the Elder Neglect Scale. Multiple linear regression analyses showed that the main personal factors influencing geriatric nursing assistants’ elder neglect were general self-efficacy (β = 0.312), proactive personality (β = 0.180), and advanced qualification (β = 0.084), while the main organizational factors included monthly salary ≤ 1,900 RMB (β = −0.256), no regular training after induction (β = −0.253), and the number of days off per month (3–4 days off β = 0.192, ≥ 5 days off β = 0.101).ConclusionAlthough geriatric nursing assistants are at low levels of elder neglect, it remains a cause for concern. Among the personal factors, geriatric nursing assistants who possessed proactive personalities, high self-efficacy and advanced qualifications, exhibited low levels of elder neglect. Among the organizational factors, those who possessed a high number of days off per month portrayed low levels of elder neglect. Conversely, those who received low monthly salaries and no regular training after induction portrayed high levels of elder neglect. To reduce the risk of elder neglect, nursing homes should give due consideration to candidates’ self-efficacy and proactive personality traits when recruiting, and focus on fostering these personality traits in their employees during their work. In addition, strengthening regular training for geriatric nursing assistants, optimizing the salary structure, and arranging rest days in a reasonable manner are also necessary measures.

To estimate the pooled prevalence of elder abuse and neglect in rural areas. In this work, the pooled prevalence of elder abuse and neglect in rural areas was 33%. For the prevalence estimates of abuse and neglect subtypes, neglect was the highest, followed by psychological abuse, financial, physical and sexual abuse. In the context of global aging, there is an urgent need for high quality studies based on agreed definition of elder abuse and neglect in order to protect the potential high risk populations. Many epidemiological studies have reported that elder abuse and neglect were prevalent in rural areas. However, none of them has synthesized the literature in this field. Therefore, we aimed to estimate the overall prevalence of elder abuse and neglect in rural areas through a systematic review and meta-analysis. PubMed, EMBASE, Web of Science, and Cochrane Library were systematically searched to identify eligible articles, with no language restrictions. Statistical analyses were conducted using Review Manager software (version 5.3). Meta-analyses and sensitivity analysis were performed using a random-effects model. All results were reported as the pooled prevalence of elder and neglect with their 95% confidence intervals (CIs). The quality of the included studies was evaluated by strengthening the reporting of observational studies in epidemiology (STROBE) checklist. Potential publication bias was assessed by the funnel plot. 13 cross-sectional studies involving 10,313 participants were eligible. The prevalence of elder abuse and neglect ranged from 4.5 to 61.7% across the rural areas, and pooled prevalence estimate was 33% (95% CI 23–43). The prevalence of physical abuse was estimated at 7% (95% CI 5–9), financial abuse at 5% (95% CI 4–7), psychological/emotional abuse at 17% (95% CI 11–23), and neglect at 26% (95% CI 17–35). There was significant heterogeneity among the included studies. Stratified analyses revealed that sampling design was part of the heterogeneity source. WHO regions, gender, countries’ income classification, and study quality could not explain the potential reasons for heterogeneity. The pooled prevalence of elder abuse and neglect was relatively high in rural areas. Early and targeted screening and prevention are needed. There is an urgent need for high quality studies using agreed definition of elder abuse and neglect to protect the potential high risk populations.

Emerging evidence suggests that gut microbiota, short-chain fatty acids (SCFAs), and inflammatory cytokines play important roles in the pathogenesis of diabetic cognitive impairment (DCI). However, little is known about alterations of gut microbiota and SCFA levels as well as the relationships between inflammatory cytokines and cognitive function in Chinese DCI patients. Herein, the differences in the gut microbiota, plasma SCFAs, and inflammatory cytokines in DCI patients and type 2 diabetes mellitus (T2DM) patients were explored. A cross-sectional study of 30 DCI patients and 30 T2DM patients without mild cognitive impairment (MCI) was conducted in Tianjin city, China. The gut microbiota, plasma SCFAs, and inflammatory cytokines were determined using 16S ribosomal RNA (rRNA) gene sequencing, gas chromatography-mass spectrometry (GC-MS), and Luminex immunofluorescence assays, respectively. In addition, the correlation between gut microbiota and DCI clinical characteristics, SCFAs, and inflammatory cytokines was investigated. According to the results, at the genus level, DCI patients presented a greater abundance of Gemmiger, Bacteroides, Roseburia, Prevotella, and Bifidobacterium and a poorer abundance of Escherichia and Akkermansia than T2DM patients. The plasma concentrations of acetic acid, propionic acid, isobutyric acid, and butyric acid plummeted in DCI patients compared to those in T2DM patients. TNF-α and IL-8 concentrations in plasma were significantly higher in DCI patients than in T2DM patients. Moreover, the concentrations of acetic acid, propionic acid, butyric acid, and isovaleric acid in plasma were negatively correlated with TNF-α, while those of acetic acid and butyric acid were negatively correlated with IL-8. Furthermore, the abundance of the genus Alloprevotella was negatively correlated with butyric acid, while that of Holdemanella was negatively correlated with propanoic acid and isobutyric acid. Fusobacterium abundance was negatively correlated with propanoic acid. Clostridium XlVb abundance was negatively correlated with TNF-α, while Shuttleworthia abundance was positively correlated with TNF-α. It was demonstrated that the gut microbiota alterations were accompanied by a change in SCFAs and inflammatory cytokines in DCI in Chinese patients, potentially causing DCI development. These findings might help to identify more effective microbiota-based therapies for DCI in the future.