Occurrence Of Cognitive Impairment Research Articles

Are demographic factors, masticatory performance and structural brain signatures associated with cognitive impairment in older people? A pilot study of cross-sectional neuroimaging data.

The occurrence of cognitive impairment (CI) is expected to increase within an ageing population. CI is associated with tooth loss, which influences masticatory performance. A decrease in masticatory performance may cause functional and morphological changes in the brain. However, whether CI is associated with masticatory performance, demographics, and structural brain signatures has not been studied yet. To assess the associations between CI on the one hand, and masticatory performance, demographic factors, and structural brain signatures (i.e. cortical volume and thickness) on the other hand. In total, 18 older adults with CI (mean ± SD age = 72.2 ± 9.5 years) and 68 older adults without CI (65.7 ± 7.5 years) were included in this study. Masticatory performance was quantified using a colour-changeable chewing gum. A Magnetic Resonance Imaging (MRI) scan was used to map structural brain signatures. To study our aim, a multivariate binary logistic regression analysis with backward selection was performed. The cortical volume of the right entorhinal cortex was negatively associated with CI (p < .01). However, demographic factors, masticatory performance, and the other structural brain signatures under investigation were not associated with CI. A decrease in the volume of the right entorhinal cortex is associated with CI in older people.

Aerobic exercise combined with memory strategy training improve the cognitive function.

Type 2 diabetes mellitus (T2DM) is closely associated with the occurrence of cognitive impairment, imposing a heavy burden on the patient's family and society. Aerobic exercise and targeted memory strategies have been widely reported to improve cognitive function. A total of 122 T2DM patients with Montreal Cognitive Assessment Scale (MoCA) test scores of less than 26 received the aerobic exercise combined with memory strategy training. After 6 months of intervention, a final group of 113 patients entered the final evaluation and analysis. Diabetes-specific quality of life scale (DSQL) and activities of daily living (ADL) assessments were performed to evaluate the life quality of the patients. The scores of MoCA and ADL were significantly upregulated, and the scores of DSQL were significantly reduced after the 6-month intervention of T2DM patients. The levels of fasting plasma glucose (FPG), hemoglobin A1c, total cholesterol (TC), and triglyceride (TG) levels of T2DM patients with cognitive impairment significantly decreased post intervention. A significant decrease in low density lipoprotein cholesterol (LDL-C) and an increase in high density lipoprotein cholesterol (HDL-C) were observed. The FPG, HbA1, TC, TG, and LDL-C levels were significantly lower, and the HDL-C levels were significantly higher in patients with normal cognitive function than in patients with abnormal cognitive function. Aerobic exercise combined with memory strategy training effectively improved the memory and cognitive function in patients with T2DM.

Alleviation of Cognitive Impairment-like Behaviors, Neuroinflammation, Colitis, and Gut Dysbiosis in 5xFAD Transgenic and Aged Mice by Lactobacillus mucosae and Bifidobacterium longum.

Neuropsychiatric disorders including Alzheimer's disease (AD) may cause gut inflammation and dysbiosis. Gut inflammation-suppressing probiotics alleviate neuropsychiatric disorders. Herein, to understand whether anti-inflammatory probiotics Lactobacillus mucosae NK41 and Bifidobacterium longum NK46, which suppressed tumor necrosis factor (TNF)-α expression in lipopolysaccharide (LPS)-stimulated macrophages, could alleviate cognitive impairment, we first examined their effects on cognitive function, gut inflammation, and gut microbiota composition in 5xFAD-transgenic mice. Oral administration of NK41 or NK46 decreased cognitive impairment-like behaviors, hippocampal amyloid-β (Aβ), TNF-α and interleukin (IL)-1β expression, hippocampal NF-κB+Iba1+ cell population, and Aβ accumulation, while hippocampal brain-derived neurotropic factor (BDNF) and IL-10 expression and BDNF+NeuN+ cell population increased. They also decreased TNF-α and IL-1β expression and NF-κB+CD11c+ cell population in the colon. They also reduced fecal and blood LPS levels and gut Proteobacteria and Verrucomicrobia populations (including Akkkermansiaceae), which are positively associated with hippocampal TNF-α and fecal LPS levels and negatively correlated with hippocampal BDNF level. However, they increased Odoribactericeae, which positively correlated with BDNF expression level and TNF-α to IL-10 expression ratio. The combination of NK41 and NK46 (4:1, NKc), which potently inhibited TNF-α expression in LPS-stimulated macrophages, additively alleviated cognitive impairment-like behaviors in 5xFAD-transgenic or aged mice. NKc increased hippocampal BDNF+NeuN+ cell population and BDNF expression in 5xFAD-transgenic or aged mice, while hippocampal TNF-α and IL-1β expression decreased. NKc also decreased TNF-α and IL-1β expression in the colon and LPS levels in the blood and feces. These findings suggest that gut bacteria and its product LPS may be closely connected with occurrence of cognitive impairment and neuroinflammation and the combination of NK41 and NK46 can additively alleviate cognitive impairment and neuroinflammation by inducing NF-κB-suppressed BDNF expression and suppressing LPS-producing gut bacteria.

Prospective observational studies on nutrition intake and the incidence of cognitive impairment in middle-aged and older adults: A protocol for systematic review and meta-analysis.

According to several studies, a specific dietary pattern can reduce the risk of dementia and cognitive impairment. However, the robustness of these results has not been tested. The study intends to investigate the association between nutrition intake and cognitive impairment in middle-aged and older adults (≥45-years) and provide reliable, evidence-based references for healthcare decision-makers, researchers, and policymakers. Are the dietary characteristics of community-dwelling adults (≥45-years) associated with the occurrence of cognitive impairment? The primary objective of this protocol is to synthesize the longitudinal observational evidence on the relationship between nutrition intake patterns and the incidence of cognitive impairment in middle-aged and older adults (≥45-years), and to provide detailed dietary recommendations for the prevention of cognitive impairment in this population. Cohort studies conducted among adults (≥45-years) will be included. The following electronic databases will be searched for relevant records published by July 2023, with a restriction on language to English: Pubmed, Medline, Embase, Web of science, Cochrane Library. The studies will be selected, the data will be extracted, and the bias risk will be assessed by two independent investigators. The Meta-analysis of Observational Studies in Epidemiology guidelines will be followed to summarize observational studies, and the protocol will adhere to the recommendations from the Preferred Reporting Items for Systematic Review and Meta-Analysis Protocols 2015 statement. Endnote X9 will be used to manage data screening. We will use Review Manager 5.4 and Stata 16.0 to conduct data analysis, and a random-effects model will be applied to pool clinically homogenous studies. The results will be presented based on the form of nutrition intake. For assessing publication bias, Egger's test and visual inspection of funnel plots will be utilized. As this study does not involve primary data, ethical approval is not required. The final report will be published in a peer-reviewed journal. A registration number of DOI 10.17605/OSF.IO/NAKC3 was assigned to it on October 15, 2022 on Prospero.

Clinical Values of Serum Uric Acid Levels in the Occurrence of Cognitive Impairment in Alcohol-Dependent Patients.

Studies have confirmed that uric acid is involved in the regulation of cognitive function. This study aimed to investigate the expression of serum uric acid in alcohol-dependent patients and evaluate its clinical diagnostic value for cognitive impairment. Blood sample was collected for assessment of serum uric acid levels. Montreal Cognitive Assessment Scale scores were obtained to assess cognitive function. Anxiety and depression scores on the Symptom Check List 90 scale were used to assess mental health status. The alcohol-dependent patients were divided into non-cognitive impairment and cognitive impairment groups according to Montreal Cognitive Assessment Scale score, and the serum uric acid levels of these groups were analyzed. The receiver operating characteristic curve evaluated the diagnostic value of serum uric acid in cognitive impairment patients. Pearson correlation coefficient evaluated the correlation between uric acid and Montreal Cognitive Assessment Scale score, anxiety score, and depression score. Multivariate logistic regression analyzed the association between each index and cognitive impairment in patients. Serum uric acid was higher in patients than in controls (P < .001). Uric acid was significantly increased in cognitive impairment patients than in non-cognitive impairment patients (P < .001). Serum uric acid has certain diagnostic value in patients with cognitive impairment. Anxiety score and depression score were positively correlated with uric acid level, while Montreal Cognitive Assessment Scale score was negatively correlated with uric acid. Additionally, serum uric acid, Montreal Cognitive Assessment Scale score, and anxiety and depression scores were the risk factors for cognitive impairment in patients (P < .05). The abnormal expression of uric acid has a high diagnostic accuracy for distinguishing cognitive impairment from non-cognitive impairment.

The Neuropsychiatric Aspect of the Chronic Viral Hepatitis.

Chronic viral hepatitis is a systemic disease characterized by a wide range of extrahepatic manifestations, such as cognitive impairment, chronic fatigue, sleep disorders, depression, anxiety and a decrease in quality of life. This article presents a summary of the main theories and hypotheses about the occurrence of cognitive impairment, features of treatment of patients with chronic viral hepatitis. Often, extrahepatic manifestations can outstrip the clinical manifestations of liver damage itself, which requires the use of additional diagnostic and treatment methods, and they can also significantly change the treatment tactics and prognosis of the disease. Changes in neuropsychological parameters and cognitive impairments are often recorded in patients with chronic viral hepatitis at stages characterized by the absence of significant liver fibrosis and liver cirrhosis. These changes usually occur regardless of the genotype of the infection and in the absence of structural damage to the brain. The purpose of this review is to study the main aspects of the formation of cognitive impairment in patients with chronic hepatitis, cirrhosis of viral etiology.

Intermediate repeat expansions of TBP and STUB1: Genetic modifier or pure digenic inheritance in spinocerebellar ataxias?

PurposeCAG/CAA repeat expansions in TBP>49 are responsible for spinocerebellar ataxia (SCA) type 17 (SCA17). We previously detected cosegregation of STUB1 variants causing SCA48 with intermediate alleles of TBP in 2 families. This cosegregation questions the existence of SCA48 as a monogenic disease. MethodsWe systematically sequenced TBP repeats in 34 probands of dominant ataxia families with STUB1 variants. In addition, we searched for pathogenic STUB1 variants in probands with expanded alleles of TBP>49 (n = 2) or intermediate alleles of TBP≥40 (n = 47). ResultsSTUB1 variants were found in half of the TBP40-49 cohort. Mirroring this finding, TBP40-49 alleles were detected in 40% of STUB1 probands. The longer the TBP repeat length, the more likely the occurrence of cognitive impairment (P = .0129) and the faster the disease progression until death (P = .0003). Importantly, 13 STUB1 probands presenting with the full SCA48 clinical phenotype had normal TBP37-39 alleles, excluding digenic inheritance as the sole mode. ConclusionWe show that intermediate TBP40-49 alleles act as disease modifiers of SCA48 rather than a STUB1/TBP digenic model. This distinction from what has been proposed before has crucial consequences for genetic counseling in SCA48.

Caffeine intake improves the cognitive performance of patients with chronic kidney disease.

ObjectiveCognitive impairment is a common complication of chronic kidney disease (CKD). Caffeine intake has been reported to improve cognitive performance in several studies. However, whether the benefits of caffeine intake on cognitive function apply to patients with CKD remains unknown.MethodsWe performed a retrospective cross-sectional study based on the National Health and Nutrition Examination Survey (NHANES). The data of CKD subjects and non-CKD subjects from NHANES 2011−2014 were analyzed. Propensity score matching (PSM) was performed based on age, sex, diabetes, cancer, educational level, energy intake and protein intake to select subjects. The Consortium to Establish a Registry for Alzheimer’s Disease Word Learning Test (CERAD-WL), the CERAD Word List Recall Test (CERAD-DR), the Animal Fluency Test (AF) and the Digit Symbol Substitution Test (DSST) were used, whereby the occurrence of cognitive impairment was identified. Logistic regression models were performed to evaluate the association between caffeine intake and cognitive performance in CKD and non-CKD participants. Stratified analyses according to the stage of CKD and the urinary albumin/creatinine ratio levels were performed. Plot curves were then generalized to present a non-linear relationship, and the inflection point for each non-linear model was obtained by using a recursive algorithm.ResultsCognitive impairment was more prevalent in CKD patients than in non-CKD subjects. For CKD patients, caffeine intake was associated with higher CERAD-WL, CERAD-DR, AF and DSST scores. For non-CKD subjects, caffeine intake was associated with higher DSST scores only. Subgroup analysis revealed that caffeine only benefited the cognitive function of patients with CKD stages 2 and 3. The analysis showed non-linear relationships of caffeine intake and cognitive function for both CKD and non-CKD subjects. The inflection point of caffeine intake for CKD patients was 279 mg/day.ConclusionThe recommended dose of caffeine intake to improve the cognitive function of CKD patients is ≤279 mg/day.

Clearing the Fog: a Systematic Review on Cognitive Dysfunction in COVID-19

[Objective] The systematic review aims to examine the association between COVID-19 and cognitive dysfunction, including the link between the severity of COVID-19 and the occurrence of cognitive impairment and the potential pathophysiological mechanisms related to brain fog among COVID-19 patients. [Methods] PubMed, Oxford University Press, ProQuest Health and Medical Complete, ScienceDirect, Ovid, HERDIN, Google Scholar, and Cochrane Library databases were accessed to retrieve literature using the PRISMA guidelines. [Results] After critical appraisal, 13 full journal articles were included in the study. The studies showed the most frequent cognitive impairment are attention, memory, and executive function in COVID-19 patients. Compared with healthy controls in three out of four studies, cognitive impairment was only evident in COVID-19 patients. Furthermore, two studies showed no correlation between brain fog and depression, and five studies showed a link between the severity of COVID-19 infection and cognitive impairment. Cases ranging from mild to severe illness presented manifestations of brain fog. However, a disparity in the evidence of the pathophysiology of COVID-19 and cognitive dysfunction exists, prompting the need to investigate further. Additionally, recent studies provide insufficient evidence for direct central nervous system invasion, and there are emerging studies that contrast the presumed pathogenesis of neurological complications from neuroinflammation. [Conclusion] There is an association between COVID-19 and cognitive dysfunction. Manifestation of cognitive dysfunction is present regardless of illness severity. Moreover, there are existing pathophysiological mechanisms of the Coronavirus that lead to cognitive dysfunction in COVID-19 patients; however, additional studies are required to substantiate such mechanisms further. [PROSPERO registration number] CRD42022325669.

The association between undiagnosed diabetes and cognitive function: findings from the China health and retirement longitudinal study

BackgroundThe cognitive function of people with diabetes has gained an increasing interest in recent years, and this study focuses on exploring the relationship between undiagnosed diabetes and cognitive function among the middle-aged and elderly people in China.MethodsThe data came from the China Health and Retirement Longitudinal Study (CHARLS) which was conducted between July and October 2015. 9855 subjects were enrolled in the study. Executive function and episodic memory were used to assess cognitive function. The subjects were divided into three groups: no diabetes, diagnosed diabetes, and undiagnosed diabetes, and weighted multiple linear regression models were established to evaluate the association of undiagnosed diabetes with cognitive function.ResultsAfter controlling for covariates, undiagnosed diabetes was statistically associated with executive function (β = −0.215, P < 0.01). In the age group of ≥65 years, undiagnosed diabetes was statistically associated with executive function (β = −0.358, P < 0.01) and episodic memory (β = −0.356, P < 0.01). When adjusting for confounders, no statistically significant associations were found between diagnosed diabetes and cognitive function except in 45-54 age group (β = 0.374, P < 0.05).ConclusionsThe cross-sectional study suggested that undiagnosed diabetes was linked to poor cognitive function, especially in the elderly population. Timely diagnosis and active treatment of diabetes are important to reduce the occurrence of cognitive impairment. Further prospective cohort studies are required to articulate the association between undiagnosed diabetes and cognitive function.

Occurrence of cognitive impairment in older adult patients with epilepsy (P17-8.001)

Occurrence of cognitive impairment in older adult patients with epilepsy (P17-8.001)

The Effect of Long-Term or Repeated Use of Antibiotics in Children and Adolescents on Cognitive Impairment in Middle-Aged and Older Person(s) Adults: A Cohort Study.

ObjectivesWe evaluated the effects of long-term/recurrent use of antibiotics in childhood on developing cognitive impairment in middle and old age from UK Biobank Database.MethodsUK Biobank recruited participants aged 37–73 years. Cognitive impairment was ascertained by fluid intelligence questionnaire. Primary outcome was the occurrence of cognitive impairment in middle and old age. Multivariate logistic regression models were used to explore the relationship between long-term/recurrent use of antibiotics and cognitive impairment.ResultsOver 3.8–10.8 years’ follow-up, 4,781 of the 35,921 participants developed cognitive impairment. The odds of cognitive impairment in middle and old age among long-term/recurrent use of antibiotics in childhood were increased by 18% compared with their counterparts (adjusted odd ratio 1.18, 95% confidence interval 1.08–1.29, p < 0.01). The effect of long-term/recurrent use of antibiotics in childhood on cognitive impairment was homogeneous across different categories of various subgroup variables such as sex, age, APOE4, ethnic groups, income before tax, smoking status, alcohol status, BMI, hypertension and diabetes but the effect of long-term/recurrent use of antibiotics in childhood was modified by the educational qualification (p-value for interaction <0.05).ConclusionLong-term/recurrent use of antibiotics in childhood may increase the risk of cognitive impairment in middle and old age.

Assessment of the Risk of Depression in Residents Staying at Long-Term Care Institutions in Poland During the COVID-19 Pandemic Depending on the Quality of Cognitive Functioning.

Background: The development of the COVID-19 pandemic has prompted the implementation of many procedures to safeguard against further increases in illness. Unfortunately, this has drastically reduced residents’ contact with their families, which has increased feelings of loneliness and isolation. This is particularly difficult in long-term care facilities, where the risk of developing depression is higher than in the general population.Objectives: The aim of the study was to assess the risk of depression among the residents of long-term care institutions in Poland during the COVID-19 pandemic and to determine the relationship between the risk of depression and the occurrence of cognitive impairment in the study group.Methods: The study included 273 residents from long-term care institutions in Poland. The risk of depression was determined based on an originally designed questionnaire. The cognitive state of the subjects was assessed using the screening test Mini-Mental State Examination (MMSE). Both the depression risk assessment and the MMSE test were conducted twice: in March and December 2020.Results: In March, severe dementia was present in 28.2% of the residents and normal MMSE scores were observed in 16.1% of the subjects; in December, the prevalence of severe dementia increased to 31.1% and that of normal scores decreased to 10.3%. In March, no participant was found to be at high risk of depression and moderate risk was observed in 14.3% of the subjects; in December, 2.6% of the residents had a high risk score and 45.4% had a moderate risk score. Statistical analysis revealed that higher MMSE scores correspond with a higher risk of depression.Conclusion: A higher risk of depression was observed with the development of the pandemic. Residents with cognitive impairment were characterised by a lower risk of depression compared to individuals with normal MMSE scores. During the study, progression of cognitive impairment was observed in the residents.

Brain architecture changes across the FTLD spectrum

AbstractBackgroundTo explore structural/functional MRI connectomic features of the motor neuron disease (MND) and behavioral variant of frontotemporal dementia (bvFTD) spectrum.Method115 MND (including amyotrophic lateral sclerosis [ALS] and primary lateral sclerosis), 35 bvFTD patients and 61 controls underwent clinical/cognitive and MRI evaluations. MND patients were divided in 79 pure‐motor (MND‐motor) and 36 cognitive/behavioral impaired (MND‐ci/bi). A sub‐analysis was performed on ALS patients only (54 ALS‐motor, 21 ALS‐ci/bi and 8 ALS‐FTD). Graph analysis and connectomics assessed structural/functional topological network properties at global, lobar and regional level.ResultGlobally, bvFTD showed altered structural and functional network properties compared to all other groups. At lobar level, bvFTD showed altered structural and functional network properties within the frontotemporal and basal ganglia areas relative to all groups. Structural alterations in the parietal lobe discriminated bvFTD from controls and MND‐motor only. MND groups showed altered structural properties within sensorimotor and basal ganglia areas relative to controls. Regionally, bvFTD showed widespread structural damage and decreased functional connectivity relative to all groups. MND showed disrupted structural architecture and enhanced functional connectivity within sensorimotor, basal ganglia and frontotemporal areas relative to controls. Similar results have been found in ALS sub‐analysis.ConclusionThe disruption of the structural architecture in MND worsens in relation with cognitive deficits. Functional changes are characterized by enhanced functional connectivity in presence of exclusive motor impairment that intensifies with the occurrence of cognitive impairment in MND. The Italian Ministry of Health (GR‐2011‐02351217; GR‐2013‐02357415; RF‐2011‐02351193), AriSLA (ConnectALS), European Research Council (StG‐2016_714388_NeuroTRACK).

Exosomal miRNA-223-3p as potential biomarkers in patients with cerebral small vessel disease cognitive impairment.

BackgroundCerebrovascular disease is a common clinical illness. Many patients with cerebrovascular disease can be accompanied by cognitive impairment. The exosomal microRNA (miRNA)-223-3p is related to vascular endothelial injury, synaptic function, inflammatory response, and other mechanisms. In this study, we investigated the levels of plasma exosomal miRNA-223-3p in patients with cerebral small vessel disease (CSVD), in order to determine whether it could be used as a more accessible potential biomarker for the early diagnosis and treatment of CSVD. This study aimed to explore whether the development of cognitive impairment can be explained by differentially expressed miRNA-223-3p by detecting the level of miRNA-223-3p, which is abundant in peripheral blood exosomes related to cognitive impairment in CSVD.MethodsThe three groups of participants included 40 patients with CSVD cognitive impairment (CSVDCI), 38 patients with CSVD, and 35 normal controls (NC). The real-time polymerase chain reaction (RT-PCR) was used to detect the expression level of blood exosomal miRNA-223-3p. In addition, we also studied the relationship between exosomal miRNA-223-3p and blood Hcy and C-reactive protein (CRP). Receiver-operating characteristic (ROC) curve analysis was used to evaluate the diagnostic efficacy of plasma exosomal miRNA-223-3p.ResultsThe expression of exosomal miRNA-223-3p in CSVD increased, and the expression of miRNA-223-3p increased significantly with the occurrence of cognitive impairment. Exosomal miRNA-223-3p was positively correlated with the expression levels of Hcy and CRP in the blood.ConclusionsThe expression of plasma exosomal miRNA-223-3p is associated with the development of cognitive impairment in patients with CSVD. It may be involved in the pathogenesis of CSVD and cognitive impairment, and can be used as a sensitive predictive biomarker.

Clinical significance of the cognition-related pathogenic proteins in plasma neuronal-derived exosomes among normal cognitive adults over 45years old with olfactory dysfunction.

Exosomal Phospho-Tau-181(P-T181-tau), Total tau (T-tau), and amyloid-β peptide 42 (Aβ42) have been proved the capacity for the amnestic mild cognitive impairment (MCI) and the diagnosis of Alzheimer's disease (AD). This study aimed to explore the cognitive function and the levels of P-T181-tau, T-tau, and Aβ42 in neuronal-derived exosomes (NDEs) extracted from plasma in normal cognitive adults over 45years old with olfactory dysfunction. A cross-sectional survey of 29 participants aged over 45 was conducted. Plasma exosomes were isolated, precipitated, and enriched by immuno-absorption with anti- L1 cell adhesion molecule (L1CAM) antibody. NDEs were characterized by CD81, and extracted NDE protein (P-T181-tau, T-tau, and Aβ42) biomarkers were quantified by enzyme-linked immunosorbent assay (ELISAs). Olfactory performance was assessed by Sniffin' Sticks and cognitive performance was assessed by Montreal Cognitive Assessment (MoCA). There was no significant difference between adults with olfactory dysfunction and without olfactory dysfunction regarding the cognitive function as measured by MoCA and all the participants showed normal cognition. Adults with olfactory dysfunction showed a higher concentration of P-T181-tau in plasma NDEs than did adults without olfactory dysfunction (P = 0.034). Both the levels of P-T181-tau (r = - 0.553, P = 0.003) and T-tau (r = - 0.417, P = 0.034) negatively correlated with the odor identification scores. In addition, the level of T-tau negatively correlated with MoCA scores (r = - 0.597, P = 0.002). The levels of P-T181-tau (r = - 0.464, P = 0.022) and T-tau (r = - 0.438, P = 0.032) negatively correlated with the delayed recall scores. This study demonstrated that cognition-related pathogenic proteins including P-T181-tau in plasma NDEs were significantly increased in adults over 45years old with olfactory dysfunction before the occurrence of cognitive impairment. The impaired odor identification and the delayed recall function were highly associated with the increased levels of P-T181-tau and T-tau in plasma NDEs.

Frequency and risk factors of post-intensive care syndrome components in a multicenter randomized controlled trial of German sepsis survivors.

Post-intensive care syndrome (PICS) is a combination of cognitive, psychiatric and physical impairments in survivors of critical illness and intensive care. There is little data on long-term co-occurrence of associated impairments. Analysis of data from 289 sepsis survivors from a German multicenter RCT. Impairments associated with PICS (depression, PTSD, cognitive impairment, chronic pain, neuropathic symptoms, dysphagia) during 24 months follow-up are used to explore the frequency and risk factors of PICS components in three classification models. The majority of participants showed impairments in 2-3 of 6 domains during follow-up. The overall frequency of PICS according to the classification models ranged from 32.9% to 98.6%. In regression analyses, there were no significant effects in selected ICU-related exposures or covariates for PICS classification models. Regarding individual components, only higher age and longer duration of ICU treatment and mechanical ventilation showed significant positive associations with the occurrence of cognitive impairment during follow-up, as did male gender and higher age for dysphagia. Almost all study participants showed impairments associated with PICS in at least one domain. The proposed classification models for PICS appear to be too broad to identify specific risk factors beyond its individual components.

A Review of Acute Coronary Syndrome and its Potential Impact on Cognitive Function.

According to the World Health Organization (WHO) forecasts, in 2030, the number of people suffering from dementia will reach 82 million people worldwide, representing a huge burden on health and social care systems. Epidemiological data indicates a relationship between coronary heart disease (CHD) and the occurrence of cognitive impairment (CI) and dementia. It is known that both diseases have common risk factors. However, the impact of myocardial infarction (MI) on cognitive function remains controversial and largely unknown. The main goal of this study is to attempt to summarize and discuss selected scientific reports on the causes, mechanisms and effects of CI in patients after acute coronary syndrome (ACS), especially after MI. The risk of CI can increase in patients after ACS, and can therefore also adversely affect the further course of treatment. A late diagnosis of CI can lead to serious clinical implications, such as an increase in the number of hospitalizations and mortality.

Disentangling the PIGD classification for the prediction of cognitive impairment in de novo Parkinson\u2019s disease

BackgroundPostural Instability and Gait difficulties (PIGD) subtype has been associated with worse cognitive performance in Parkinson’s disease (PD).ObjectiveTo investigate whether PIGD subtype classification or PIGD-related clinical features predict the development of cognitive decline in de novo PD patients.MethodsData from 422 PD patients with de novo PD were obtained from the PPMI database. At follow-up (up to 6 years), patients were categorized as having cognitive impairment or not. Multivariate Cox survival analysis was carried out including motor subtype and individual MDS-UPDRS items defining PIGD phenotype as predictors. Previously validated clinical predictors of cognitive impairment were included in the model as covariates. Occurrence of cognitive impairment at follow-up was used as the time-to-event and Kaplan–Meier curve was generated.ResultsAt baseline, 76 patients were classified as PIGD, 299 tremor-dominant and 47 as indeterminate. Development of cognitive impairment was not associated with PIGD subtype (p = 0.252). When individual MDS-UPDRS items were interrogated in the model, postural instability proved to be an independent predictor of cognitive impairment (HR = 2.045; 95%CI: 1.068–3.918; p = 0.031), while gait difficulties were not associated with cognitive decline (p = 0.870).ConclusionsOur findings suggest that postural instability, as assessed by MDS-UPDRS III, may serve as a possible indicator of the risk of developing cognitive impairment in de novo PD patients rather than the PIGD phenotype.

COGNITIVE IMPAIRMENT IN HYPERTENSIVES

Background: Hypertension and dementia increase parallel to age. Objective: The purpose of this study was to study the effect of hypertension on cognition before age-related cognitive impairment begins to set in. Methods: In this prospective, cross-sectional study conducted at a tertiary-care centre between May 2014 and December 2015, 300 (150 hypertensives and 150 normotensives) participants were compared. Patients were divided into groups according to age, gender, education, and duration of hypertension. The Hindi Mini-Mental State Examination (HMMSE) was used to detect cognitive impairment. Results: Overall, occurrence of cognitive impairment was 53 (35.3%) in hypertensives and 37 (24.7%) in normotensives. Below 60 years male and female hypertensives and normotensives had comparable mean HMMSE scores, although not statistically significant. Sixty years and above male and female normotensives achieved slightly higher HMMSE scores than male and female hypertensives, however this finding was statistically significant (p=0.002) for males ≥60 years. Among the cognitive domains, orientation to time (p=0.009), registration (p=0.018), recall (p=0.031), and 3 step command (p=0.014) were statistically different between hypertensives and normotensives. Periventricular white matter ischemia was discovered in 8 (5.3%) and 2 (1.3%) hypertensives and normotensives, respectively. Conclusion: Although hypertension was not statistically associated with cognitive decline in hypertensives &lt;60 years, hypertensives &gt;60 years showed statistical significance with cognitive decline. Furthermore, specific cognitive domains such as orientation to time, registration, recall, and 3 step command displayed statistical significance for cognitive decline. Future prospective, large-scale studies are warranted to investigate these and other possible associations.