Risk Factor For Cognitive Dysfunction Research Articles

An analysis of factors influencing cognitive dysfunction among older adults in Northwest China based on logistic regression and decision tree modelling

BackgroundCognitive dysfunction is one of the leading causes of disability and dependence in older adults and is a major economic burden on the public health system. The aim of this study was to investigate the risk factors for cognitive dysfunction and their predictive value in older adults in Northwest China.MethodsA cross-sectional study was conducted using a multistage sampling method. The questionnaires were distributed through the Elderly Disability Monitoring Platform to older adults aged 60 years and above in Northwest China, who were divided into cognitive dysfunction and normal cognitive function groups. In addition to univariate analyses, logistic regression and decision tree modelling were used to construct a model to identify factors that can predict the occurrence of cognitive dysfunction in older adults.ResultsA total of 12,494 valid questionnaires were collected, including 2617 from participants in the cognitive dysfunction group and 9877 from participants in the normal cognitive function group. Univariate analysis revealed that ethnicity, BMI, age, educational attainment, marital status, type of residence, residency status, current work status, main economic source, type of chronic disease, long-term use of medication, alcohol consumption, participation in social activities, exercise status, social support, total scores on the Balanced Test Assessment, total scores on the Gait Speed Assessment total score, and activities of daily living (ADL) were significantly different between the two groups (all P < 0.05). According to logistic regression analyses, ethnicity, BMI, educational attainment, marital status, residency, main source of income, chronic diseases, annual medical examination, alcohol consumption, exercise status, total scores on the Balanced Test Assessment, and activities of daily living (ADLs) were found to influence cognitive dysfunction in older adults (all P < 0.05). In the decision tree model, the ability to perform activities of daily living was the root node, followed by total scores on the Balanced Test Assessment, marital status, educational attainment, age, annual medical examination, and ethnicity.ConclusionsTraditional risk factors (including BMI, literacy, and alcohol consumption) and potentially modifiable risk factors (including balance function, ability to care for oneself in daily life, and widowhood) have a significant impact on the increased risk of cognitive dysfunction in older adults in Northwest China. The use of decision tree models can help health care workers better assess cognitive function in older adults and develop personalized interventions. Further research could help to gain insight into the mechanisms of cognitive dysfunction and provide new avenues for prevention and intervention.

Assessment of cognitive dysfunction and its influencing factors after acute ischemic stroke

Objective In order to provide a more accurate and effective basis for clinical diagnosis and treatment, patients with cognitive dysfunction after acute ischemic stroke (AIS) were evaluated and their influencing factors were analyzed. Methods A rigorous and systematic logistic regression analysis was conducted to comprehensively investigate the various influencing factors that contribute to cognitive dysfunction. Results Among them, the sex granulocyte/lymphocyte ratio (NLR), low-density lipoprotein cholesterol (LDL-C) level, and C-reactive protein (CRP) were also higher than those in the control group (p < 0.05). The scores of memory, orientation, visual and spatial function, abstract thinking and language in the control group were higher than those in the experimental group (p < 0.05). The results of multivariate logistic regression analysis showed that history of diabetes mellitus, high NLR, high LDL-C, high CRP, smoking and temporal lobe infarction were risk factors for cognitive dysfunction after AIS, while elevated BMI and love of exercise were protective factors for cognitive dysfunction after AIS. Conclusion Patients with cognitive dysfunction had the highest incidence of temporal lobe infarction, and they scored lower than the control group on memory, orientation, visual and spatial function, abstract thinking, and language function. Multivariate logistic regression analysis showed that a history of diabetes mellitus, high NLR, high LDL-C, high CRP, smoking, and temporal lobe infarction were independent risk factors for cognitive dysfunction after acute ischemic stroke, while elevated BMI and a love of exercise were protective factors for cognitive dysfunction after acute ischemic stroke.

Correlation between risk factors of cognitive dysfunction and blood pressure variability after acute ischemic stroke in northwest Shanghai

： Objective: To explore the relationship between risk factors of cognitive dysfunction and blood pressure variability after acute ischemic stroke in northwest Shanghai to establish a model for early identification of high-risk groups of cognitive dysfunction and formulation of more targeted prevention and treatment measures. Methods: Spearman test was used to evaluate the correlation between blood pressure variability and Montreal Cognitive Assessment (MoCA) score in patients with acute ischemic stroke and the partial regression coefficient model was constructed based on the above independent risk factors, and the receiver operating characteristic (ROC) curve was described to analyze the relevant independent risk factors. Results: ROC curve analysis results showed that the clinical prediction model was significantly more effective than a single factor in predicting the risk of cognitive impairment after acute ischemic stroke in northwest Shanghai（P < 0.05）. Conclusion: Cognitive dysfunction after acute ischemic stroke was closely related to high Homocysteine (Hcy) levels, high standard deviation of systolic blood pressure, previous infarction history and infarction of cognitive function area in northwest Shanghai. The prediction model based on the above factors showed satisfactory value in predicting of cognitive dysfunction risk after acute ischemic stroke and there was also the correlation between cognitive function and blood pressure variability.

Risk factors and characteristics analysis of cognitive impairment in patients with cerebral infarction during recovery period

Objective To analyze the risk factors and characteristics of cognitive impairment in patients with cerebral infarction during the recovery period. Methods This retrospective case-control study included 183 patients with cerebral infarction in the recovery period. According to the MMSE score, they were divided into a cognitive impairment group of 79 cases and a cognitive normal group of 104 cases. Collect clinical data from all patients, including age, gender, body mass index, laboratory test results, past medical history, National Institute of Health Stroke Scale (NIHSS) score, modified Barthel index, Oxfordshire Community Stroke Project (OCSP) classification, and number of infarcted lesions. Multiple logistic regression analysis was used to identify risk factors related to cognitive impairment in patients with cerebral infarction. Result There were significant differences (p < 0.05) between the cognitive impairment group and the cognitive normal group in terms of age, body mass index, low-density lipoprotein level, NIHSS score, modified Barthel index, and number of infarcted lesions. Multivariate logistic regression analysis showed that age ≥ 65 years, stroke, carotid artery plaques, NIHSS score ≥ 5, anterior circulation infarction type, and multiple infarcted lesions were important risk factors for cognitive impairment. Conclusion Elderly age, presence of carotid artery plaques, high NIHSS score, multiple infarct lesions, and specific infarct types are important risk factors for cognitive dysfunction in patients during the recovery period of cerebral infarction.

Lower cognitive reserve is related to worse working memory performance in older adults after mTBI. An ERP study

ABSTRACT Objective Older adults (OA) after mild traumatic brain injury (mTBI) have a high risk of developing persistent post-injury cognitive impairments. Lower pre-morbid cognitive reserve (CR) is increasingly investigated as a risk factor for cognitive dysfunction in OA. However, how CR protects against effects of mTBI at the brain level remains largely understudied. Methods We examined 22 OA who sustained mTBI (mean 67.69 years, SD 5.11) in the sub-acute phase and 15 age- and CR-matched healthy OA (mean 68 years, SD 5.55) performing a three-level visual N-back task using electroencephalography. We calculated inverse efficiency scores of performance from accuracy and reaction times. Event-related potentials served as neurocognitive correlates of attentional (P2) and working memory (P3) processing. Results Overall, mTBI OA performed worse than healthy OA (p = 0.031). Lower CR generally decreased performance (p < 0.001). Furthermore, with increasing task difficulty, task performance was more affected by CR (p = 0.004). At the brain level, P2 amplitude was lower in mTBI OA than in healthy OA (p = 0.05). There was no clear effect of CR on P2 or P3 measures. Conclusion As mTBI OA with lower CR performed worse on a working-memory task, lower CR may be a risk factor for worse recovery after mTBI in this group.

Evaluation of Impact of Low Hb, MCV, MCHC and MCH on Cognitive Ability of Undergraduated Medical Students

Introduction: Low concentrations of hemoglobin or anemia can contribute chronic brain hypoxia and reduced aerobic capacity, thus increasing the risk of dementia or cognitive decline. From the clinical point of view, brain ischemia is a known risk factor of cognitive dysfunction and dementia. We investigated correlation and impact of low Hb, MCV, MCHC and MCH on cognitive abilities from 386 participants on 59 top 10 undergraduate medical students. Objective: This study aimed to determine and evaluate the correlation and impact of low Hb, MCV, MCHC and MCH on cognitive abilities of 59 top 10 undergraduated medical students in Ahmad Shah Abdali Higher Education Institute of Khost province of Afghanistan. Method and Materials: It is prospective descriptive cross sectional study, on 59 top 10 undergraduated medical students in Ahmad Shah Abdali Higher Education Institute of Khost province from 2023/ Oct / 12 to 2023/ Nov / 02. The including parameters were Hb, MCV, MCHC and MCH of all 386 participants under study that recorded in computer special format. Hb, MCV, MCHC and MCH are done by special regents and micro lab. Recorded findings processing, comparison and evaluation results have been identified by IBM SPSS-23 version. Results: The study was conducted during (20) days on 386 undergraduated medical students in Ahmad shah Abdali Higher Education Institute of Khost province. Initially we described all male participants according to age. At the current study all male participants were with (mean age: 23.14 ± 3.68; range: 20-45 years). All participants of this study were from all (1st, 2nd, 3rd, 4th, 5th and 6th) classes. Statistic description of all participants, according to Hb, MCV, MCHC and MCH shows that normal range of Hb level for male (14-16.6g/dl) was more prevalent 301(77.97). Low level of Hb for male (Low ˂ 13.5g/dl) was 19(4.92) and high level of Hb for male (High &gt; 16.6g/dl) was 66(17.09).The normal range of MCV (80-95%) was 327(84.71), low range (Low ˂80) was 54(13.98) and high range (High&gt;95%) was 5(1.29).The normal range of MCHC (32-36%) was 370(95.85), low range (Low ˂ 32) was 15(3.88) and high range (High&gt;36%) was 1(0.25).The normal range of MCH (23-31%) was 322(83.41), low range (Low ˂ 23) was 19(4.92) and high range (High&gt;31%) was 5(11.65). In the second part of this study we described all above parameters in the group of all 59 top 10 participants students for comparative outcomes. Statistic description of 59 top 10 participants, according to Age, Hb, MCV, MCHC and MCH shows that at the current study top 10 participants were with (mean age 23.40± 2.78; range: 18-32 years). Normal range of Hb level for male (14-16.6g/dl) was 43(72.88). Low level of Hb for male (Low ˂ 13.5g/dl) was 2(3.38) and high level of Hb for male (High &gt; 16.6g/dl) was 14(23.72). The normal range of MCV (80-95%) was 51(86.44), low range (Low ˂80) was 8(13.55) and high range (High&gt;95%) was 0(0). The normal range of MCHC (32-36%) was 57(96.61), low range (Low ˂ 32) was 2(3.38) and high range (High&gt;36%) was 0(0).The normal range of MCH (23-31%) was 50(84.74), low range (Low ˂ 23) was 2(3.38) and high range (High&gt;31%) was 7(11.86).Pearson correlation between Hb and MCV is at the 0.01 level significant, (P&lt;0.00). Conclusion: Overall, findings of our study indicated that, low Hb, MCV, MCHC and MCH have significant correlation with cognitive ability of undergraduated students. However, this issue needs to further investigations to confirm these findings.

Reduced skeletal muscle mass to visceral fat area ratio is independently associated with reduced cognitive function in type 2 diabetes mellitus

AimSkeletal muscle mass to visceral fat area ratio (SVR) has been recognised as an index of sarcopenic obesity. SVR is associated with type 2 diabetes mellitus (T2DM), metabolic syndrome and arterial stiffness which are known risk factors for cognitive dysfunction. We aimed to investigate association between SVR and cognitive function in patients with T2DM. MethodsThis was a cross-sectional study of 1326 patients with T2DM and mean age 61.3 ± 8.0 years. SVR was assessed based on bioelectrical impedance measurements of muscle mass and visceral fat area (VFA). Cognitive function was assessed using Repeatable Battery for the Assessment of Neuropsychological Status (RBANS). Linear regression was used to examine the association between SVR in quartiles and RBANS score, adjusting for demographics, education, presence of depressive symptoms, clinical covariates and medications. ResultsThe lower SVR quartiles were negatively associated with RBANS total score in the unadjusted analysis. The corresponding coefficients for Quartiles 1 and 2 SVR were −3.79 (95 % CI −5.39 to −2.19; p < 0.001) and −1.47 (95 % CI −2.86 to −0.07; p = 0.039) in fully adjusted analysis. The negative association between Quartile 1 SVR and RBANS score was evident in immediate memory, delayed memory, visuo-spatial construction, language and attention domains. Muscle mass and VFA alone had weaker associations with RBANS scores. ConclusionOur study demonstrated, for the first time, an independent association between reduced SVR and lower cognitive function. This is evident in global and multiple cognitive domains. The synergistic effects of reduced muscle mass and visceral obesity may be more pronounced than their independent effects on cognitive function.

Changes in mild cognitive impairment and sociodemographic disparity among adults aged 55 years and above in 4 provinces of China

To investigate the changes in mild cognitive impairment(MCI) and sociodemographic disparity among adults aged 55 years and above in 4 provinces of China. A total of 4687 adults aged 55 years and above from Community-based Cohort Study on Nervous System Disease who did not have Alzheimer&apos;s disease, participated in both rounds of the survey, and had complete baseline sociodemographic data and two rounds of data on cognitive function were selected. Generalized estimation equations were used to analyse the effect of sociodemographic factors on MCI. The detection rates of MCI in adults aged 55 years and above without Alzheimer&apos;s disease in 4 provinces of China in 2018 and 2020 were 48.56% and 42.56% respectively. MCI occurred in 30.11% of those with normal cognition(NC) at baseline, and 44.24% of those with MCI at baseline reverted to NC. The risk of MCI increased and the likelihood of MCI reversion decreased with increasing age and decreasing per capita monthly household income. In the baseline NC population, the risk of MCI in the junior high school and above group was 35% lower than that in the illiterate group(RR=0.65, 95%CI 0.53-0.80), the risk of MCI was lower in those living in rural areas(RR=0.56, 95%CI 0.49-0.65), and the risk of MCI was 1.17 times(95%CI 1.03-1.32) higher in those with a history of chronic diseases than in those without it. In the baseline MCI population, the likelihood of MCI reversion increased with education, the likelihood of MCI reversion was 1.04 times higher for workers than for non-workers(95%CI 1.00-1.08). The incidence and reversal rates of MCI were high in adults aged ≥55 years in four provinces of China. Advanced age, low education and low income level are risk factors for cognitive dysfunction.

Promotion of neuroinflammation by the glymphatic system: a new insight into ethanol extracts from Alisma orientale in alleviating obesity-associated cognitive impairment.

Obesity is one of the critical risk factors for cognitive dysfunction. The glymphatic system (GS) plays a key role in the pathogenesis of cognitive deficits. Alisma orientale has been shown to have anti-inflammatory and antihyperlipidemic effects, whereas its effects and underlying mechanisms on obesity-associated cognitive impairment (OACI) are unclear. This work aims to decipher the mechanism of ethanol extracts from Alisma orientale (EEAO) in restoring cognitive impairment in HFD-induced obese mice through a GS approach. The restoration of abnormal glucose/lipid metabolism and excess adipose deposition by EEAO were assayed by biochemical analysis and visually displayed by a micro-CT scanner and Oil Red O staining. Biochemical assays and Western blotting (WB) were used to measure cerebral blood flow (CBF), free fatty acid (FFAs) levels and the structural integrity of the blood-brain barrier (BBB). Microglial activation and neuroinflammation were assessed with immunohistochemistry staining, ELISA and WB. Moreover, GS function was determined by immunofluorescence staining, fluorescence tracer imaging and WB. Finally, the neuropathological features and cognitive functions were detested with immunohistochemistry staining, immunofluorescence and Morris Water Maze. EEAO not only alleviated body weight, cerebral lipid accumulation and serum FFAs in HFD-induced obese mice, but also increased CBF and BBB integrity. EEAO suppressed microglial activation and lipid deposition in the hippocampus and reduced the level of inflammatory cytokines including IL-6, IL-1β and TNF-α in brain tissue. Interestingly, long-term HFD-induced GS dysfunction was significantly restored after EEAO intervention, and neuropathological lesions and cognitive deficits were also markedly rescued. EEAO rescued the cognitive deficits of OACI by inhibiting neuroinflammation and restoring GS dysfunction, indicating a potential remedy for OACI.

Correlation between long-term glycemic variability and cognitive function in middle-aged and elderly patients with type 2 diabetes mellitus: a retrospective study.

To investigate the correlation between long-term glycemic variability and cognitive function in middle-aged and elderly patients with type 2 diabetes mellitus (T2DM). This retrospective analysis includes 222 patients hospitalized at Second Affiliated Hospital of Anhui Medical University from June 2021 to June 2023. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA) and Mini-Mental State Examination (MMSE). All patients were categorized into the MCI group and the non-MCI group based on their MoCA score. Long-term blood glucose fluctuations were measured using glycated hemoglobin A1c standard deviation (HbA1c-SD) and fasting plasma glucose standard deviation (FPG-SD). The study compared general clinical data, blood biochemical indicators, and glycemic variability indicators between the two groups. The differences between the groups were compared using t-test, Chi-Square Test, or Mann-Whitney U test. Kendall's correlation analysis, multivariate logistic regression analysis and ROC curve correlation analysis were further used to analyze the correlation and diagnostic power. The differences in age, MoCA scores, MMSE scores, HOMA-β, HbA1c-M, HbA1c-SD, FPG-M, FPG-SD, eGFR, Smoking, GLP-1RA and SGLT-2i usage were statistically significant between the two groups (P<0.05). Kendall's correlation analysis showed that age, HbA1c-M, HbA1c-SD, FPG-M, and FPG-SD was negatively correlated with MoCA scores; meanwhile, the HOMA-β, and eGFR was positively correlated with MoCA scores. Multiple logistic regression analysis revealed that HbA1c-SD, FPG-SD and Smoking were risk factors for cognitive dysfunction, while eGFR, GLP-1RA and SGLT-2i usage was a protective effect. The area under the curve (AUC) values for predicting MCI prevalence were 0.830 (95% CI [0.774-0.877], P<0.001) for HbA1c-SD, 0.791 (95% CI [0.655-0.808], P<0.001) for FPG-SD, and 0.698 (95% CI [0.633-0.757], P<0.001) for eGFR. The optimal diagnostic values were 0.91, 1.32, and 74.81 ml/min/1.73 m2 for HbA1c-SD, FPG-SD, and eGFR, respectively. Cognitive function in middle-aged and elderly T2DM patients is influenced by long-term blood glucose variability, with poorer cognitive function observed in individuals with higher blood glucose variability. The impact of HbA1c-SD on MCI exhibited a greater magnitude compared to that of PFG-SD and smoking. Additionally, renal function, GLP-1RA and SGLT-2i usage exert positive effects on cognitive function.

Is adiponectin deficiency a critical factor for sevoflurane induced neurocognitive dysfunction?

The global rise in obesity has resulted in an increase in the number of surgical procedures under general anaesthesia in this patient population. Sevoflurane is one of the most widely used volatile aesthetic agent in developed countries. Clinical evidence suggests obesity is a risk factor for cognitive dysfunction after surgery. Experimentally animals with pre-existing cerebral insults are more susceptible to the neurotoxic effects of sevoflurane compared with their normal counterparts. Nevertheless, the mechanism underlying this vulnerability in obese subjects is not fully elucidated.Obesity is associated with a significant reduction of adiponectin, an adipocyte-derived molecule with neurotrophic and anti-inflammatory properties. Adiponectin receptors are abundantly expressed in hippocampus and cortex. Moreover, adiponectin deficiency is associated with exacerbation of neuroinflammation, neuronal dysfunction and cognitive impairment in animal models of obesity and Alzheimer’s disease. Based on these observations, we hypothesize that adiponectin deficiency plays a critical role in sevoflurane induced cognitive dysfunction in obese subjects accounting for its higher incidence in this patient population. With diminished protective effects from adiponectin, sevoflurane may further exacerbate neuroinflammation by activating the proinflammatory pathways and increase the synthesis of inflammatory cytokines in the brain, leading to significant neuronal dysfunction and cognitive impairment. On the other hand, treatment with adiponectin or adiponectin receptor agonists may have therapeutic potential in minimizing the risk of postoperative cognitive impairment in obese patients undergoing surgery. As an oral adiponectin agonist is available, it can be expeditiously evaluated in clinical trials if our hypothesis is validated.

Metabolic Syndrome Score is Associated with Lower Myelin in Cognitively Healthy Adults

AbstractBackgroundMetabolic syndrome (MetS) is a cluster of cardiovascular risk factors, including abdominal obesity, glucose intolerance, elevated blood pressure (BP), and dyslipidemia. MetS is a known risk factor for cognitive dysfunction and dementia (Yaffe et al., 2004. YAMA), and has been linked to brain atrophy and altered WM microstructure measured with diffusion tensor MR (Alfaro et al., 2018, Metabolism). The metabolic cost of myelin maintenance makes WM particularly vulnerable to metabolic dysfunction. Here, we aim to explore the relationships between MetS and myelin, as well as test whether WC‐myelin association (Bouhrara et al., 2021, Int J Obes) is independent from systolic BP.MethodSample included 90 cognitively and neurologically healthy adults (Bookheimer et al., 2019, Neuroimage), aged 20 to 79 (M = 53, SD = 17) with 76% women. Additional exclusion criteria included systolic blood pressure &gt;140, BMI&gt;33, and &gt;2 on modified Hachinski Ischemic Scale. Myelin water imaging was collected using a 3T Siemens Skyra with a 32‐channel coil and 3D‐gradient and spin‐echo (GRASE) sequence (1.9×1.9×4mm, TR = 1000ms, echoes = 32, first echo = 10ms, echo spacing = 10ms). Myelin Water Fraction maps were nonlinearly aligned to FMRIB58_FA using TBSS in FSL. MetS score was calculated as a sum of z‐scored waist circumference (WC), systolic BP, BMI, and self‐reports history of elevated cholesterol and glucose.ResultA linear regression analysis with MWF as the dependent variable, adjusting for sex, race, ethnicity, age, and age2, income and education, indicated that greater MetS score was associated with lower MWF in several regions including the genu corpus callosum, anterior corona radiata, and external capsule. WC was negatively associated with whole WM MWF (B = ‐.265, t(79,9) = ‐2.150, p = 0.035) after controlling for the above covariates and systolic BP.ConclusionAssociations between MetS with myelin content were detected especially in the late‐myelinating regions. This aligns with the development‐to‐degeneration hypothesis of WM aging, with lower oligodendrocyte‐to‐axon ratio as a possible factor contributing to metabolic vulnerability of late‐myelinating tracts. We also replicated the WC‐myelin association, although in fewer regions and with smaller effects sizes. Together, our results suggest that different metabolic syndrome components may exert both additive/synergistic, and independent effects on myelin integrity across adulthood.

Probiotic Clostridium butyricum ameliorates cognitive impairment in obesity via the microbiota-gut-brain axis

Obesity is a risk factor for cognitive dysfunction and neurodegenerative disease, including Alzheimer's disease (AD). The gut microbiota-brain axis is altered in obesity and linked to cognitive impairment and neurodegenerative disorders. Here, we targeted obesity-induced cognitive impairment by testing the impact of the probiotic Clostridium butyricum, which has previously shown beneficial effects on gut homeostasis and brain function. Firstly, we characterized and analyzed the gut microbial profiles of participants with obesity and the correlation between gut microbiota and cognitive scores. Then, using an obese mouse model induced by a Western-style diet (high-fat and fiber-deficient diet), the effects of Clostridium butyricum on the microbiota-gut-brain axis and hippocampal cognitive function were evaluated. Finally, fecal microbiota transplantation was performed to assess the functional link between Clostridium butyricum remodeling gut microbiota and hippocampal synaptic protein and cognitive behaviors. Our results showed that participants with obesity had gut microbiota dysbiosis characterized by an increase in phylum Proteobacteria and a decrease in Clostridium butyricum, which were closely associated with cognitive decline. In diet-induced obese mice, oral Clostridium butyricum supplementation significantly alleviated cognitive impairment, attenuated the deficit of hippocampal neurite outgrowth and synaptic ultrastructure, improved hippocampal transcriptome related to synapses and dendrites; a comparison of the effects of Clostridium butyricum in mice against human AD datasets revealed that many of the genes changes in AD were reversed by Clostridium butyricum; concurrently, Clostridium butyricum also prevented gut microbiota dysbiosis, colonic barrier impairment and inflammation, and attenuated endotoxemia. Importantly, fecal microbiota transplantation from donor-obese mice with Clostridium butyricum supplementation facilitated cognitive variables and colonic integrity compared with from donor obese mice, highlighting that Clostridium butyricum’s impact on cognitive function is largely due to its ability to remodel gut microbiota. Our findings provide the first insights into the neuroprotective effects of Clostridium butyricum on obesity-associated cognitive impairments and neurodegeneration via the gut microbiota-gut-brain axis.

Risk factors for cognitive dysfunction and glycemic management in older adults with type 2 diabetes mellitus: a retrospective study

BackgroundEpidemiological evidence shows a robust relationship between cognitive dysfunction and type 2 diabetes mellitus (T2DM). This study identified major risk factors that might prevent or ameliorate T2DM-associated cognitive dysfunction in the realm of clinical practice.MethodsUsing Mini-mental State Examination (MMSE) in the light of education level, we identified older adults with T2DM on admission aged 50 and above. We conducted this case–control study when eligible participants were divided into Cognitively Normal (CN) group and Cognitively Impaired (CI) group. Analytical data referred to demographic characteristics, clinical features, fluid biomarkers, and scale tests.ResultsOf 596 records screened, 504 cases were included in the final analysis. Modified multivariate logistic regression analysis verified that homocysteine (OR = 2.048, 95%CI = 1.129–3.713), brain infarction (OR = 1.963, 95%CI = 1.197–3.218), dementia (OR = 9.430, 95%CI = 2.113–42.093), education level (OR = 0.605, 95%CI = 0.367–0.997), severity of dependence (OR = 1.996, 95%CI = 1.397–2.851), creatine kinase (OR = 0.514, 95%CI = 0.271–0.974) were significant risk factors of incident T2DM-related cognitive dysfunction in patients of advanced age.ConclusionOur study supported a robust relationship between T2DM and cognitive dysfunction. Our results provide clinicians with major risk factors for T2DM-related cognitive dysfunction, in particular the protective role of creatine kinase.

Serum levels of 25-OH vitamin D levels predict cognitive impairments among acute coronary syndrome patients.

The cognitive impairment after percutaneous coronary intervention (PCI) in patients with acute coronary syndrome (ACS) has become a crucial clinical concern that cannot be ignored. However, studies on the early warning factors of cognitive impairment after PCI are still insufficient. This study reviewed the postoperative cognitive function of 284 patients who underwent PCI in our hospital from June 2019 to June 2022. During the 21-day follow-up, all participants included in the analysis were divided into the cognitive impairment (CI) group (n = 82) and the noncognitive impairment (NCI) group (n = 186) according to their Montreal cognitive assessment (MoCA) scale. Participants' serum 25(OH)D3 levels on admission and serum neuron-specific enolase (NSE), glial fibrillary acidic protein (GFAP) and S100β levels were measured 21 days after surgery. Age more than 65 years, hypertension, operation time longer than 60 min, left ventricular ejection fraction less than 50% and serum 25(OH)D3 less than 31.41 ng/ml were the risk factors for cognitive dysfunction in ACS patients 21 days after PCI. Serum levels of 25(OH)D3, NSE, S100β and GFAP were significantly higher in patients with cognitive impairment than in patients without cognitive impairment. Postoperative serum NSE, S100β and GFAP levels were significantly negatively correlated with serum 25(OH)D3 levels at admission. The serum 25(OH)D3 level is a risk factor and predictor of cognitive impairment in patients with ACS after PCI.

Neurocognitive Functioning of Patients with Sinonasal and Nasopharyngeal Cancers Treated With Multimodality Therapy

Abstract Importance Few recent studies have examined neurocognitive functioning (NCF) in patients with sinonasal and nasopharyngeal cancers (NPCs) prior to and following multimodality therapy or the potential differences in NCF by disease variables such as disease site. Objective The objective of this study is to determine rates of NCF impairments prior to and following multimodality therapy, declines in NCF following radiotherapy (RT), and possible differences in NCF by the disease site. Design, Setting, and Participants We conducted a retrospective chart review of 39 patients with sinonasal and NPCs who underwent comprehensive neuropsychological evaluations. Twenty patients were evaluated prior to RT, of which eleven received follow-up evaluation after completion of RT. Nineteen patients were evaluated following various treatments without a pre-RT evaluation. Main Outcomes and Measures Patients completed comprehensive neuropsychological evaluations. Decline from pre-RT to follow-up was defined on the basis of reliable change indices. Results Thirty-nine patients completed comprehensive neuropsychological evaluations. For the entire cohort, the most frequently demonstrated impairments were in verbal memory (47%) and learning (43%), executive functioning (33%), and verbal fluency (22%). At post-RT follow-up, the most frequently observed declines were in verbal learning (46%) and memory (18%). Demographic and disease variables were not significantly associated with NCF at pre-RT or post-RT. Conclusion and Relevance Patients with sinonasal and NPCs are at risk for NCF impairments in multiple areas at baseline and memory decline following RT. Future prospective studies are needed to investigate the impact of each treatment modality on NCF and specific risk factors for cognitive dysfunction.

Incidence and risk factors of cognitive dysfunction in hemodialysis patients: A systematic review and meta-analysis.

The study aims to explore the incidence and risk factors of cognitive dysfunction in hemodialysis patients. PubMed, Embase, Cochrane Library, and Web of Science databases were searched for clinical studies on the association between hemodialysis and cognitive dysfunction from the database's inception to 1 December 2022. Two researchers independently completed data extraction and risk of bias assessments for the included studies. All statistical analyses were performed using STATA15.0 software. Ten studies were included in this meta-analysis, with a total of 5535 hemodialysis patients, that is, 2033 patients with cognitive dysfunction and 3502 patients with normal cognitive function. The Newcastle-Ottawa Scale scores of the included studies were greater than 5. Meta-analysis results suggested that the incidence of cognitive dysfunction in hemodialysis patients was (effect size = 51%, 95% confidence interval [CI] [0.33, 0.69]), and hemodialysis patients with cognitive dysfunction were often older than those with normal cognition (standard mean difference [SMD] = 0.49, 95% CI [0.31, 0.68]). Female gender was a risk factor for cognitive dysfunction in hemodialysis patients (relative risk [RR] = 1.21, 95% CI [1.04, 1.41]); diabetes (RR = 1.33, 95% CI [1.04, 1.71]) and stroke (RR = 1.66, 95% CI [1.08, 2.55]) increased the incidence of cognitive dysfunction in hemodialysis patients. The most important risk factors for cognitive dysfunction associated with hemodialysis might be female gender, old age, diabetes, and stroke. Close attention should be paid to such patients for early prevention.

Arteriolosclerosis CSVD: a common cause of dementia and stroke and its association with cognitive function and total MRI burden.

Arteriolosclerosis cerebral small vessel disease (CSVD) is a common type of CSVD. This study aimed to explore the factors associated with cognitive function and total MRI burden related to the disease. The demographic characteristics, clinical manifestations, cognitive function score, Barthel Index (BI), blood test index, and follow-up results of arteriolosclerosis CSVD patients treated for the first time in our hospital from January 2014 to August 2022 were collected. White matter hyperintensity (WMH) Fazekas score, total MRI burden, and cerebral atrophy grade were evaluated according to brain MRI findings. Factors associated with CSVD cognitive function were analyzed by binary logistic regression. The correlative factors related to the total MRI burden of CSVD were analyzed by ordered multiple logistic regression. A total of 146 patients were included in this study, of which 132 cases (90.4%) had hypertension. There were 108 patients (74.0%) with cognitive dysfunction, 97 patients (66.4%) with balance and gait disorders, and 83 patients (56.8%) with moderate-to-severe dependence in daily life (BI ≤ 60 points). Of 146 patients, 79 (54.1%) completed clinical and imaging follow-ups for a median of 3 years. The number of patients with cognitive impairment and BI ≤ 60 points after follow-up significantly increased compared with the first admission (P < 0.001). There were also significant differences in total MRI burden (P = 0.001), WMH Fazekas score, and cerebral atrophy grade (P < 0.001). Mean age (P = 0.012), median deep WMH Fazekas score (P = 0.028), and median deep (P < 0.001) and superficial (P =0.002) cerebral atrophy grade of patients with cognitive impairment at first admission were all higher than those with non-cognitive impairment. Multivariate analysis showed that deep cerebral atrophy was independently and significantly associated with cognitive impairment of CSVD (P = 0.024), and hypertension was significantly and independently associated with total MRI burden (P = 0.001). The disease course of arteriolosclerosis CSVD may be related to cognitive function and total MRI burden. Deep cerebral atrophy was an independent risk factor for cognitive dysfunction in arteriolosclerosis CSVD, and hypertension was an independent risk factor for total MRI burden.

Resolvin E1 ameliorates diabetes‐related cognitive impairment via ChemR23

AbstractBackgroundDiabetes mellitus (DM) is an independent risk factor for cognitive dysfunction. The resolvin E1 (RvE1)/ChemR23 axis is involved in the progression and complications of DM. However, the impact of the RvE1/ChemR23 axis on diabetes‐related cognitive impairment remains unclear.MethodAging‐related behavioral changes in db/db diabetic mice and age‐matched nondiabetic controls were assessed, and changes of ChemR23 in the hippocampus were studied.ResultThe results showed that db/db mice exhibited age dependent learning and memory impairments in the Morris water maze test, along with reduced expression of ChemR23 in the hippocampus compared with age‐matched wild‐type mice. Moreover, neuronal damage, oxidative stress, and neuroinflammation were also observed in db/db mice. A moderate dose of RvE1 for 4 weeks elicited a significant reduction in memory loss, along with reduced neuronal damage, alleviation of oxidative stress, and attenuated neuroinflammation in diabetic mice but not in ChemR23‐knockout diabetic mice.ConclusionCollectively, our study suggested that RvE1 could ameliorate DM‐related cognitive dysfunction by reducing oxidative stress and neuroinflammation in a ChemR23‐dependent manner.

Diabetes mellitus type 2 as an underlying, comorbid or consequent state of mental disorders

Somatic disturbances that occur in parallel with psychiatric diseases are a major challenge in clinical practice. Various factors contribute to the development of mental and somatic disorders. Type 2 diabetes mellitus (T2DM) is a significant health burden worldwide, and the prevalence of diabetes in adults is increasing. The comorbidity of diabetes and mental disorders is very common. By sharing a bidirectional link, both T2DM and mental disorders influence each other in various manners, but the exact mechanisms underlying this link are not yet elucidated. The potential mechanisms of both mental disorders and T2DM are related to immune and inflammatory system dysfunction, oxidative stress, endothelial dysfunction, and metabolic disturbances. Moreover, diabetes is also a risk factor for cognitive dysfunction that can range from subtle diabetes-associated cognitive decline to pre-dementia and dementia. A complex re-lationship between the gut and the brain also represents a new therapeutic approach since gut-brain signalling pathways regulate food intake and hepatic glucose production. The aim of this minireview is to summarize and present the latest data on mutual pathogenic pathways in these disorders, emphasizing their complexity and interweaving. We also focused on the cognitive performances and changes in neurodegenerative disorders. The importance of implementing integrated approaches in treating both of these states is highlighted, along with the need for individual therapeutic strategies.