Risk Factor For Cognitive Impairment Research Articles

Postoperative cognitive dysfunction in heart transplantation recipients.

This study aimed to investigate the occurrence and risk factors of postoperative neurocognitive disorder (NCD) in patients who underwent heart transplantation. Seventy-six heart transplant patients were analyzed for clinical data including gender, age, height, weight, education level, left ventricular ejection fraction (LVEF), stroke volume (SV), transplantation duration, and pretransplant medical history. Cognitive function was assessed using the mini-mental status examination (MMSE) and Montreal cognitive assessment (MoCA) scales. Patients were categorized into cognitively normal and impaired groups based on the presence or absence of cognitive dysfunction, and their cognitive function scores were compared. Multivariate logistic regression was used to identify independent risk factors for cognitive impairment in postoperative cardiac transplant patients. Cognitive dysfunction was observed in 48 out of 76 heart transplant patients, representing an incidence of 63.2%. Cognitive impairment in heart transplant recipients predominantly affected multiple cognitive domains. Logistic regression analysis identified age (OR=1.057, 95% CI 1.002-1.115), gender (OR=.200, 95% CI.044-.919), education level (OR=.728, 95% CI.600-.883), LVEF (OR=.891, 95% CI.820-.969), and history of diabetes (OR=7.674, 95% CI 1.317-44.733) as independent risk factors for postoperative NCD in heart transplant recipients (P<.05). The study found a high incidence of postoperative NCD in heart transplant patients, with gender, age, education level, LVEF, and diabetes history being significant risk factors. Early identification and intervention targeting these risk factors may help prevent NCD in postheart transplant patients and improve long-term outcomes.

Anticholinergic and sedative medication use in older patients with cognitive concerns.

Anticholinergic (AC) and sedative medications are a risk factor for cognitive impairment. This study sought to characterize AC and sedative use in older patients seen for outpatient neuropsychological evaluation and evaluate their associations with different cognitive domains. We hypothesized that AC and sedative use would be associated with worse attention/processing speed (AP), executive functioning (EF), and memory. We conducted a cross-sectional chart review of 392 patients (mean [M] age = 72 ± 7.7 years, range = 54-91). Medications were characterized by number of AC medications (≥1 on the Anticholinergic Cognitive Burden Scale [ACB]), number of sedative medications, and polypharmacy (≥5 daily medications). Demographically adjusted composites were calculated for AP, EF, and memory. Bivariate Pearson correlations assessed relationships between medication use and cognition. Multivariate linear regressions evaluated significant medication-cognition associations, controlling for total medications, medical comorbidities, and estimated premorbid cognitive functioning. Polypharmacy was common (80%; n = 314). Most patients (70%; n = 275) used ≥1 sedative medications (range = 0-9). Over half (63%; n = 248) used ≥1 AC drugs (range = 0-7), yet ACB scores were ≤2 in 74% of patients. Sedative use was negatively correlated with AP (r = -0.134, p = 0.008) and EF (r = -0.105, p = 0.04). ACB scores were negatively correlated with AP (r = -0.106, p = 0.037). Sedatives and a priori covariates significantly predicted AP performance (R2 = 0.127, p < 0.001); using more sedative medications was uniquely associated with worse AP (β = -0.426, p = 0.049). No significant associations were found with memory. AC and sedative medications and polypharmacy were prevalent in this sample of older patients. Though both drug classes had negative relationships with AP and EF, sedatives had a particularly negative association with AP. Contrary to our hypotheses, memory was not associated with medication use; however, anticholinergic burden was low within the sample, and AP and EF deficits may masquerade as memory problems.

Prevalence of Cognitive Impairment and Risk Factors among Elderly in Rawalpindi, Pakistan: A cross-Sectional study

Objective: The study aimed to find out the prevalence of cognitive impairment and risk factors among elderly. Study Design and setting: Descriptive cross-sectional study was conducted in elderly population of Rawalpindi. Methodology: The study was conducted from October 2020 to February 2021. After getting approval from the ethical committee, data was collected using a semi structured questionnaire. The sample of 446 participants, raised through nonprobability convenient sampling technique. Participants aged above 60 years, both genders were included however individuals who had severe head injury, depression, severe hearing and visual impairment, delirium and not willing to participate were excluded from study. Informed consent was obtained from all participants. Data was analyzed by using SPSS v24. Results: Overall mean age of sample was 69±4.6 years. Overall prevalence of cognitive impairment was 35.4 %. Among them 134 (30%) had mild cognitive impairment and 24 (5.4%) had dementia. The prevalence of cognitive impairment increases with age being higher (64.2%) at 70 years and above than at 60-69 years of age. Females 82 (61%) had high prevalence of MCI than males 52 (39%). Age, gender, hypertension, diabetes, and physical activity were significantly associated with cognitive impairment. Data was analyzed using SPSS version 24. Descriptive statistics were applied. Pearson chi square of independence was used to find the association of various factors. The p value less than 0.05 was considered significant. Conclusion: Cognitive impairment increases with the increasing age and was more prevalent among females. Hypertension, Diabetes, physical activity were modifiable risk factors for cognitive impairment

Cholinergic hyperintensity pathways are associated with cognitive performance in patients with asymptomatic carotid artery stenosis

ObjectivesWe aimed to determine whether asymptomatic carotid artery stenosis (ACS) induced cognitive impairments were related to the cholinergic hyperintensity pathway. MethodsThis cross-sectional study included patients with moderate-to-severe ACS, who were categorized into mild cognitive impairment (MCI) and normal cognition groups on the basis of Montreal Cognitive Assessment (MoCA) scores. The cholinergic pathway hyperintensity scale (CHIPS), Fazekas, and medial temporal atrophy (MTA) scores were assessed. SPSS software was used for statistical analyses. ResultsA total of 117 ACS patients (70.89 ± 8.81 years) and 105 controls (67.87 ± 9.49 years) were evaluated (t = 2.46, p = 0.015). The ACS group showed a worse median Mini-Mental Status Examination (MMSE) score (z = −2.41, p = 0.016) and MoCA score (z = −3.51, p < 0.001), and a significantly higher median total CHIPS score (z = 4.88, p < 0.001) and mean Fazekas score (t = 2.39, p = 0.018). In the correlation analysis, the MoCA score showed a significant negative correlation with the CHIPS score (ρ = −0.41, p < 0.001) and Fazekas score (ρ = −0.31, p < 0.001) in ACS group. Logistic regression analyses suggested that CHIPS scores were risk factors for MCI in patients with ACS (odds ratio [OR] = 1.07, 95% Confidence Interval [CI]1.01–1.13 and controls (OR = 1.09, 95%CI 1.01–1.17), while the MTA and Fazekas scores showed no predictive power. The receiver operating characteristic curve showed that the area under the curve of the CHIPS score for predicting MCI was 0.71 in ACS group, but was only 0.57 in controls. ConclusionsPatients with ACS showed poorer cognitive performance and higher CHIPS and Fazekas scores. CHIPS, but not Fazekas, scores were risk factors for cognitive impairment and were a valuable factor to predict MCI in patients with ACS.

Cerebral-cognitive reserve: concept and functions of the cerebral-cognitive reserve

IntroductionThe modern understanding of AD allows us to consider it through the constructs of “vulnerability” and “stability” of the brain as a dynamic system of dialectical interaction between the pathogenic process and the protective process that prevents neurodegeneration. The concept of cognitive reserve (CR) is based on observations of discrepancy between the degree of brain pathology and the severity of clinical manifestations. The concept of “reserve” was proposed to describe the resistance of the brain to a developing damage caused by a pathological process. Stern (2002) considered CR as a protective factor that modifies the impact of brain pathology on cognitive function. The researchers have defined CR as an ability to optimize cognitive function through differential involvement of structures or neural networks of the brain into brain activity.ObjectivesA systematic review of scientific studies has been conductedMethodsThe review includes an analysis of full-text literature sources.ResultsSeveral possible directions of CR influence on cognitive functions have been described:1)CR may reduce the risk of MCI or dementia through mechanisms, which do not depend on the level of neurodegenerative pathological changes in the brain.2)CR can interact with the markers of brain pathology or healthaffectingthe future cognitive decline or risk of progression. It has been found that smaller volumes or thickness in some AD vulnerable areas of the brain represent a stronger risk factor for cognitive impairment in people with low CR than in people with higher CR. CR protective effects on clinical outcomes reduce as the number of damaged neurons increases.3)The protective effect of CR increasesduring late AD onset and at a low rate of the damaged substrate accumulation.4)CR changes the relationship between genetic factors and aging withclinical and cognitive outcomes. The relationship between age and AD pathology level or age-related structural changes in the brain may weaken in people with higher CR ConclusionsThe concept of cerebral-cognitive reserve actualizes the problem of the search for compensatory mechanisms of cognitive deficit in AD, the assessmentof the structure of the reserve, the development and implementationof programs to maintain the reserve, the preventionof its depletion, starting from the preclinical stage of the disease, which can prevent the transformation of preclinical manifestations of AD into cognitive disordersDisclosure of InterestNone Declared

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.

Interactive effects of hearing aid use and cognitive function in patients with hearing loss.

There has been a significant increase in scientific investigations of the hearing-dementia association among the research on potentially modifiable risk factors for cognitive impairment. We tested two clinical questions. Analysis 1: does persistent hearing aid (HA) use decrease the decline in cognitive function caused by ageing? Analysis 2: does cognitive function at the time of HA fitting predict future persistent HA use? This case-control study performed at two referral centres reported data obtained over a 4.5-year period. We recruited a group of patients with cognitive decline, aged 65 or older with or without hearing loss. The intervention consisted of the use of HAs. The primary outcome measures were adherence to continuous HA use and cognitive function measured using the Japanese version of the Mini-Mental State Examination Test and the Reading Cognitive Test Kyoto. Eighteen HA users and 18 controls were included in the first analysis. HA use was associated with a deceleration of cognitive decline 12 months later. In the second analysis, 11 participants with good adherence to HA use were compared with 12 participants who showed poor adherence to HA use. Among the variables employed in this study, cognitive function measured using the Reading Cognitive Test Kyoto was significantly lower in participants with poor adherence to HA. HA use in cognitively impaired individuals with hearing loss can slow age-related cognitive decline. Cognitively impaired people with hearing loss who fail to commit to HA use tend to have lower cognitive measurement scores before HA fitting. HA use is generally more challenging as people age and their cognitive abilities decline. Therefore, it is desirable that HAs be used when hearing loss and dementia are in their early stages.

Low 25-Hydroxyvitamin D Increases the Risk of Cognitive and Emotional Disorders Among Chinese Patients with Cerebral Small Vessel Disease

The association between 25-hydroxyvitamin D and cognitive impairment and emotional disorder in patients with cerebral small vessel disease is unknown. This retrospective study included, 504 Chinese patients with cerebral small vessel disease admitted to the Department of Neurology of the First Hospital of Hebei Medical University between June 2019 and October 2021. The Montreal Cognitive Assessment and Hamilton Anxiety Scale (14 items) scores were utilized to divide the patients into four groups. The multivariate Cox regression analysis revealed that low 25-hydroxyvitamin D, high homo-cysteine, hyperuricemia, severity of white matter lesions, and a history of hypertension were independent risk factors for cognitive impairment among patients with cerebral small vessel disease. However, a high level of education is a protective factor. Furthermore, the level of 25-hydroxyvitamin D was significantly associated with the changes in brain functional regions. Serum 25-hydroxyvitamin D is a promising biomarker for predicting cognitive and emotional disorders in patients with cerebral small vessel disease and is highly associated with alterations in brain functional regions.

Prediction model for mild cognitive impairment in patients with type 2 diabetes using the autonomic function test.

Type 2 diabetes mellitus (T2DM) is a risk factor for cognitive impairment, and reduced heart rate variability (HRV) has been correlated with cognitive impairment in elderly individuals. This study investigated risk factors and validated a predictive model for mild cognitive impairment (MCI) in patients with T2DM using an autonomic function test. Patients with T2DM, 50-85years of age, who attended the diabetes clinic at Gyeongsang National University Hospital between March 2018 and December 2019, were included. A total of 201 patients had been screened; we enrolled 124 patients according to the inclusion and exclusion criteria in this study. Cognitive function was assessed using the Montreal Cognitive Assessment-Korean version (MOCA-K); MCI was defined as a total MOCA-K score ≤ 23. Risk factors for MCI in patients with T2DM, including demographic- and diabetes-related factors, and autonomic function test results, were analyzed. Based on multivariate logistic regression, a nomogram was developed as a prediction model for MCI. Thirty-nine of 124 patients were diagnosed with MCI. Age, education, and decreased cardiovagal function were associated with a high risk for MCI, with cardiovagal function exerting the greatest influence. However, diabetes-related factors, such as glycemic control, duration of diabetes, or medications, were not associated with the risk for MCI. The nomogram demonstrated excellent discrimination (area under the curve, 0.832) and was well calibrated. Approximately one-third of patients had MCI; as such, carefully evaluating cognitive function in elderly T2DM patients with reduced HRV is important to prevent progression to dementia.

Risk Factors for Cognitive Impairment in Multiple Sclerosis Patients

Cognitive impairment is one of the most significant burdens among the many neurological complaints in multiple sclerosis patients. Cognitive deficits negatively impact these patients’ quality of life, leading to partial or total loss of several mental functions, such as learning, memory, perception, or problem-solving. While the precise mechanisms involved in the onset and evolution of cognitive decline remain unknown, several risk factors have been associated with intellectual disability. With increasing data on this topic in recent years, the main aim of this review is to summarize the most relevant risk factors correlated with cognitive impairment in multiple sclerosis patients. Firstly, the authors demonstrate the importance of mental disability based on epidemiological data from multiple sclerosis patient cohorts. Subsequently, the intensely debated major risk factors for cognitive decline are discussed, with brief insights into the pathophysiology and possible underlying mechanisms. Finally, the authors describe the impact of medication on cognitive impairment in multiple sclerosis patients, highlighting the main research directions for future studies.

The role of neurovascular coupling dysfunction in cognitive decline of diabetes patients.

Neurovascular coupling (NVC) is an important mechanism to ensure adequate blood supply to active neurons in the brain. NVC damage can lead to chronic impairment of neuronal function. Diabetes is characterized by high blood sugar and is considered an important risk factor for cognitive impairment. In this review, we provide fMRI evidence of NVC damage in diabetic patients with cognitive decline. Combined with the exploration of the major mechanisms and signaling pathways of NVC, we discuss the effects of chronic hyperglycemia on the cellular structure of NVC signaling, including key receptors, ion channels, and intercellular connections. Studying these diabetes-related changes in cell structure will help us understand the underlying causes behind diabetes-induced NVC damage and early cognitive decline, ultimately helping to identify the most effective drug targets for treatment.

Peripheral amyloid-β clearance mediates cognitive impairment in non-alcoholic fatty liver disease

BackgroundNon-alcoholic fatty liver disease (NAFLD) is a prevalent risk factor for cognitive impairment. Cerebral amyloid-β (Aβ) accumulation, as an important pathology of cognitive impairment, can be caused by impaired Aβ clearance in the periphery. The liver is the primary organ for peripheral Aβ clearance, but the role of peripheral Aβ clearance in NAFLD-induced cognitive impairment remains unclear. MethodsWe examined correlations between NAFLD severity, Aβ accumulation, and cognitive performance in female Sprague-Dawley rats. The impact of NAFLD on hepatic Aβ clearance and the involvement of low-density lipoprotein receptor-related protein 1 (LRP-1) were assessed in rat livers and cultured hepatocytes. Additionally, a case-control study, including 549 NAFLD cases and 549 controls (782 males, 316 females), investigated the interaction between NAFLD and LRP-1 rs1799986 polymorphism on plasma Aβ levels. FindingsThe severity of hepatic steatosis and dysfunction closely correlated with plasma and cerebral Aβ accumulations and cognitive deficits in rats. The rats with NAFLD manifested diminished levels of LRP-1 and Aβ in liver tissue, with these reductions inversely proportional to plasma and cerebral Aβ concentrations and cognitive performance. In vitro, exposure of HepG2 cells to palmitic acid inhibited LRP-1 expression and Aβ uptake, which was subsequently reversed by a peroxisome proliferator-activated receptor α (PPARα) agonist. The case-control study revealed NAFLD to be associated with an increment of 8.24% and 10.51% in plasma Aβ40 and Aβ42 levels, respectively (both P <0.0001). Moreover, the positive associations between NAFLD and plasma Aβ40 and Aβ42 levels were modified by the LRP-1 rs1799986 polymorphism (P for interaction = 0.0017 and 0.0015, respectively). InterpretationLRP-1 mediates the adverse effect of NAFLD on peripheral Aβ clearance, thereby contributing to cerebral Aβ accumulation and cognitive impairment in NAFLD. FundingMajor International (Regional) Joint Research Project, National Key Research and Development Program of China, National Natural Science Foundation of China, and the Angel Nutrition Research Fund.

Resveratrol prevents cognitive deficits induced by sleep deprivation via modulating sirtuin 1 associated pathways in the hippocampus.

Accumulating evidence confirms that sleep insufficiency is a high risk factor for cognitive impairment, which involves inflammation and synaptic dysfunction. Resveratrol, an agonist of the Sirt1, has demonstrated anti-inflammation and neuroprotective effects in models of Alzheimer's disease, Parkinson's disease, and schizophrenia. However, the beneficial effects of resveratrol on sleep deprivation-induced cognitive deficits and its underlying molecular mechanisms are unclear. In the present study, thirty-two male C57BL/6 J mice were randomly divided into a Control+DMSO group, Control+Resveratrol group, SD+DMSO group, and SD+Resveratrol group. The mice in the SD+Resveratrol group underwent 5 days of sleep deprivation after pretreatment with resveratrol (50 mg/kg) for 2 weeks, while the mice in the SD+DMSO group only underwent sleep deprivation. After sleep deprivation, we evaluated spatial learning and memory function using the Morris water maze test. We used general molecular biology techniques to detect changes in levels of pro-inflammatory cytokines and Sirt1/miR-134 pathway-related synaptic plasticity proteins. We found that resveratrol significantly reversed sleep deprivation-induced learning and memory impairment, elevated interleukin-1β, interleukin-6, and tumor necrosis factor-α levels, and decreased brain-derived neurotrophic factor, tyrosine kinase receptor B, postsynaptic density protein-95, and synaptophysin levels by activating the Sirt1/miR-134 pathway. In conclusion, resveratrol is a promising agent for preventing sleep deprivation-induced cognitive dysfunction by reducing pro-inflammatory cytokines and improving synaptic function via the Sirt1/miR-134 pathway.

Executive and memory dysfunction related to binge drinking in stroke survivors during a 9-year follow-up.

Ischemic stroke and heavy alcohol consumption are both known risk factors for cognitive impairment. The issue gains importance because the prevalence of stroke and binge drinking have both increased among working-aged adults. Alarmingly, a recent cross-sectional study suggests the additive negative effects of binge drinking and comorbid brain disease on cognition. However, the long-term cognitive prognosis of the additive effects of stroke and binge drinking on adults remains unknown. In this prospective, two-center cohort study, we recruited consecutive 18-65-year-old patients with first-ever ischemic stroke along with demographically matched stroke-free controls. Patients participated in neuropsychological assessment at 6 months, 2 years, and 9 years after stroke, and in neurological assessment at acute care and at 9-year follow-up. Controls participated in a similar follow-up procedure. We examined the association between binge drinking, follow-up time, and long-term cognitive outcomes using repeated-measures analysis of variance. We included 85 patients who had had their first-ever and only ischemic stroke (mean age 53 years at the incident stroke). Patients were divided into binge-drinking (n = 22) and non-binge-drinking groups (n = 63) based on the shortened version of the Alcohol Use Disorders Identification Test. Follow-up data in healthy controls (n = 31) was used to normalize the patients' test scores for effects of age, sex, and education. We compared cognitive changes between binge-drinking and non-binge-drinking patients over a 9-year follow-up. Non-binge-drinking patients outperformed binge-drinking patients across all follow-up points on most of the executive function tests and in one memory test: binge drinking had a significant main effect both on executive function (the phonemic fluency task, p = 0.002; the Trail Making Test, p = 0.013) and memory (the list learning task, p = 0.002). Binge drinking was associated with executive and memory dysfunction at three time points over a decade after a first-ever ischemic stroke. Subdiagnostic binge drinking might increase the adverse effects of a first-ever ischemic stroke on executive function and memory, evident over a decade poststroke.

Cognitive impairment in Chinese traumatic brain injury patients: from challenge to future perspectives.

Traumatic Brain Injury (TBI) is a prevalent form of neurological damage that may induce varying degrees of cognitive dysfunction in patients, consequently impacting their quality of life and social functioning. This article provides a mini review of the epidemiology in Chinese TBI patients and etiology of cognitive impairment. It analyzes the risk factors of cognitive impairment, discusses current management strategies for cognitive dysfunction in Chinese TBI patients, and summarizes the strengths and limitations of primary testing tools for TBI-related cognitive functions. Furthermore, the article offers a prospective analysis of future challenges and opportunities. Its objective is to contribute as a reference for the prevention and management of cognitive dysfunction in Chinese TBI patients.

Assessing quality of life in childhood cancer survivors at risk for hearing loss: a comparison of HEAR-QL and PROMIS measures.

Childhood cancer survivors (CCS) exposed to platinum chemotherapy are at an increased risk of developing hearing loss and reporting decreased quality of life (QOL). This study compared two QOL measures; one developed for children with hearing loss, The Hearing Environments and Refection on Quality of Life (HEAR-QL), and one validated in CCS, the Patient-Reported Outcomes Measurement Information System (PROMIS), to assess their ability to evaluate QOL deficits in this population. Subject eligibility were restricted to CCS exposed to platinum-based chemotherapy but who were free of known risk factors for cognitive impairment, (non-central nervous system tumor, no cranial radiation, or intrathecal chemotherapy). Participants had to be between 8-17 years, have completed anti-cancer therapy for at least 6 months, and have an audiogram within 1 year, Participants completed the HEAR-QL-26 (7-12 years) or the HEAR-QL-28 (13-18 years) and the PROMIS. Independent samples and/or one sample T-tests were utilized to compare participants with normal hearing and hearing loss, and to compare outcome measures to normative HEAR-QL and PROMIS data. Non-parametric correlations were utilized to evaluate the relationship between QOL and demographic and medical variables, and QOL and severity of hearing loss. Fifty-four CCS were evaluable. The mean age was 12.0 years. Twenty-eight participants (51.9%) received cisplatin, 30 (55.6%) carboplatin, and 4 (7.4%) received both. Twenty participants (37%) demonstrated hearing loss. Participants with hearing loss scored significantly lower on the HEAR-QL than those with normal hearing (mean: 70.3, SD: 21.7, vs mean: 88.0, SD: 9.3, p =.004 for the HEAR-QL-26; mean: 84.7, SD: 10.2 vs mean: 94.8, SD: 3.4, p =.040 for the HEAR-QL-28). Participants with normal hearing scored significantly lower on the HEAR-QL-26 than the normative mean (mean: 88, SD: 9.3, normative mean: 98, SD: 5, p =.000). The PROMIS failed to identify any differences in QOL between participants based on hearing status, or when compared to the normative mean. The HEAR-QL was more sensitive than the PROMIS in identifying QOL deficits in CCS at risk for hearing loss. The HEAR-QL should be considered in studies seeking to improve the QOL of CCS with hearing loss.

The Impact of Type 2 Diabetes on Peripheral and Cerebral Hemodynamic Responses to Active Stand.

Although type 2 diabetes mellitus (T2DM) is an established risk factor for cognitive impairment, the underlying mechanisms remain poorly explored. One potential mechanism may be through effects of T2DM on cerebral perfusion. The current study hypothesized that T2DM is associated with altered peripheral and central hemodynamic responses to orthostasis, which may in turn be associated with cognitive impairment in T2DM. A novel use of function-on-scalar regression, which allows the entire hemodynamic response curve to be modeled, was employed to assess the association between T2DM and hemodynamic responses to orthostasis. Logistic regression was used to assess the relationship between tissue saturation index (TSI), T2DM, and cognitive impairment. All analyses used cross-sectional data from Wave 3 of The Irish Longitudinal Study on Ageing (TILDA). Of 2984 older adults (aged 64.3 ± 8.0; 55% female), 189 (6.3%) had T2DM. T2DM was associated with many features that are indicative of autonomic dysfunction including a blunted peak heart rate and lower diastolic blood pressure. T2DM was associated with reduced TSI and also with greater odds of impaired performance on the Montreal Cognitive Assessment (odds ratio [OR]: 1.62; confidence interval [CI: 1.07, 2.56]; p = .019). Greater TSI was associated with lower odds of impaired performance (OR: 0.90, CI [0.81-0.99]; p = .047). T2DM was associated with impaired peripheral and cerebral hemodynamic responses to active stand. Both T2DM and reduced cerebral perfusion were associated with impaired cognitive performance. Altered cerebral perfusion may represent an important mechanism linking T2DM and adverse brain health outcomes in older adults.

Risk factors for cognitive impairment in patients with chronic kidney disease.

Chronic kidney disease (CKD) patients have been found to be at risk of concurrent cognitive dysfunction in previous studies, which has now become an important public health issue of widespread concern. To investigate the risk factors for concurrent cognitive dysfunction in patients with CKD. This is a prospective cohort study conducted among patients with CKD between October 2021 and March 2023. A questionnaire was formulated by literature review and expert consultation and included questions about age, sex, education level, per capita monthly household income, marital status, living condition, payment method, and hypertension. Logistic regression analysis showed that patients aged 60-79 years [odds ratio (OR) = 1.561, P = 0.015] and ≥ 80 years (OR = 1.760, P = 0.013), participants with middle to high school education (OR = 0.820, P = 0.027), divorced or widowed individuals (OR = 1.37, P = 0.032), self-funded patients (OR = 2.368, P = 0.008), and patients with hypertension (OR = 2.011, P = 0.041) had a higher risk of cognitive impairment. The risk of cognitive impairment was lower for those with a college degree (OR = 0.435, P = 0.034) and married individuals. The risk factors affecting cognitive dysfunction are age, 60-79 years and ≥ 80 years; education, primary school education or less; marital status, divorced or widowed; payment method, self-funded; hypertension; and CKD.

Association between Dyslipidaemia and Cognitive Impairment: A Meta-Analysis of Cohort and Case-Control Studies.

This study explored the specific relationship between different lipid indicators and cognitive impairment and aimed to provide a reference for implementing targeted lipid regulation measures to prevent and alleviate cognitive impairment. We searched three databases (PubMed, Embase, and Web of Science) for literature related to hyperlipidaemia, lipid levels, and cognitive impairment, and used the Newcastle-Ottawa Scale to evaluate the quality of the identified literature. A meta-analysis was performed using RevMan 5.4, and the combined effect size ratio using a random-effects model (odds ratio [OR] and 95% confidence interval [CI]) was used to evaluate the association between dyslipidaemia and cognitive impairment. Among initially identified 2247 papers, we ultimately included 18 studies involving a total of 758,074 patients. The results of the meta-analysis revealed that patients with hyperlipidaemia had a 1.23-fold higher risk of cognitive impairment than those with normal lipid levels (OR = 1.23, 95% CI: 1.04-1.47, p = 0.02). Further subgroup analysis showed that elevated total cholesterol (TC) levels increased the risk of cognitive impairment by 1.59-fold (OR = 1.59, 95% CI: 1.27-2.01, p < 0.0001) and were more significant in older or male patients. Moreover, elevated triglyceride levels were inversely correlated with cognitive disorders, whereas elevated low-density lipoprotein cholesterol levels were unrelated to cognitive impairment risk. Dyslipidaemia was strongly associated with cognitive impairment, and elevated TC levels were a risk factor for cognitive impairment. Furthermore, the damaging effects of elevated TC levels on cognition were more pronounced in older and male populations.

Effects of DPP4 Inhibitors as Neuroprotective Drug on Cognitive Impairment in Patients with Type 2 Diabetes Mellitus: A Meta-Analysis and Systematic Review.

Type 2 diabetes mellitus is considered as one of the risk factors for cognitive impairment. DPP4 inhibitors are effective drugs for the treatment of type 2 diabetes mellitus. However, the relationship between DPP4 inhibitors and cognitive dysfunction remains unclear. Therefore, we used a meta-analysis to determine the association between DPP4 inhibitors and cognitive impairment in type 2 diabetes mellitus. We systematically searched PubMed, CNKI, and the Cochrane Library at the time of establishment, 2022, and then made inclusion criteria and screened strategies to identify studies with more precise correlations. We included 10 studies with 5,583 participants. The data showed that DPP4 inhibitors significantly reduced the incidence rate of cognitive impairment in type 2 diabetes mellitus (SMD: 0.99; 95% CI [0.59, 1.38]). Furthermore, there was a linear correlation found between cognitive impairment in type 2 diabetes mellitus and fasting blood glucose, 2-hour postprandial blood glucose, and glycosylated hemoglobin. DPP4 inhibitors decreased fasting blood glucose (FPG) (SMD: 0.52; 95% CI [-0.68, -0.37]), blood glucose (2hPPG) at 2 hours after the meal (SMD: 0.82; 95% CI, [-1.2, -0.43]), and HbA1c (SMD: 0.34; 95% CI [-0.48, -0.21]). All data were statistically significant (P < 0.0001). Furthermore, we conducted subgroup analyses of the following measures at various treatment durations and ages: cognitive scores, fasting blood glucose, glycosylated hemoglobin, and two-hour postprandial blood glucose. DPP4 inhibitors significantly improved type 2 diabetic mellitus individuals' cognitive impairment and reduced fasting blood glucose, 2-hour postprandial blood glucose, and glycosylated hemoglobin. Subgroup analysis showed that people aged 60 to 70 years had better treatment effects at 0-180 days. This trial is registered with CRD42023399473.