Cognitive Impairment In Patients Research Articles

Ketamine-dependent patients with persistent psychosis have higher neurofilament light chain levels than patients with schizophrenia

ObjectivesKetamine can induce persisting psychosis in a subset of individuals who use it chronically and heavily. Previously, we found that the psychopathology and cognitive impairments in patients with ketamine dependence (KD) exhibiting persistent psychosis (KPP) bear resemblances with schizophrenia, albeit with less severity in those with no persistent psychosis (KNP). Furthermore, we also showed that patients with KD had higher blood levels of neurofilament light chain (NFL), a biomarker for neuroaxonal injury, compared to healthy controls. In this study, we aimed to investigate the differences in NFL levels between patients with KPP and KNP while comparing the levels of individuals with schizophrenia and healthy controls. MethodsWe enrolled 64 treatment-seeking ketamine-dependent patients (53 with KNP and 11 with KPP), 37 medication-free patients with schizophrenia, and 80 healthy controls. Blood NFL levels were measured by single molecule array immunoassay. ResultsNFL levels were highest in the KPP subgroup, followed by the KNP subgroup, and then the schizophrenia and control groups (mean ± SD: 24.5 ± 24.7, 12.9 ± 10.9, 9.2 ± 12.2, and 6.2 ± 2.2 pg/mL, respectively), with no significant difference observed between the schizophrenia and control groups. ConclusionsWe found that KD is associated with higher NFL levels compared to schizophrenia, with the KPP subgroup showing the most consistent alterations. The observation of accentuated neuroaxonal pathology in individuals with KPP implies that this clinical manifestation is associated with a specific neurobiological phenotype, despite prior evidence suggesting syndromal similarity between schizophrenia and KPP.

Identification of profiles associated with conversions between the Alzheimer’s disease stages, using a machine learning approach

BackgroundThe identification of factors involved in the conversion across the different Alzheimer’s disease (AD) stages is crucial to prevent or slow the disease progression. We aimed to assess the factors and their combination associated with the conversion across the AD stages, from mild cognitive impairment to dementia, at a mild, moderate or severe stage and to identify profiles associated with earliest/latest conversion across the AD stages.MethodsIn this study conducted on the real-life MEMORA cohort data collected from January 1, 2013, and December 31, 2019, three cohorts were selected depending on the baseline neurocognitive stage from a consecutive sample of patients attending a memory center, aged between 50 and 90 years old, with a diagnosis of AD during the follow-up, and with at least 2 visits at 6 months to 1 year of interval. A machine learning approach was used to assess the relationship between factors including socio-demographic characteristics, comorbidities and history of diseases, prescription of drugs, and geriatric hospitalizations, and the censored time to conversion from mild cognitive impairment to AD dementia, from the mild stage of dementia to the moderate or severe stages of AD dementia, and from the moderate stage of AD dementia to the severe stage. Profiles of earliest/latest conversion compared to median time to conversion across stages were identified. The median time to conversion was estimated with a Kaplan-Meier estimator.ResultsOverall, 2891 patients were included (mean age 77±9 years old, 65% women). The median time of follow-up was 28 months for mild cognitive impairment (MCI) patients, 33 months for mild AD dementia and 30 months for moderate AD dementia. Among the 1264 patients at MCI stage, 61% converted to AD dementia (median time to conversion: 25 months). Among the 1142 patients with mild AD dementia, 59% converted to moderate/severe stage (median time: 23 months) and among the 1332 patients with moderate AD dementia, 23% converted to severe stage (Q3 time to conversion: 22 months). Among the studied factors, cardiovascular comorbidities, anxiety, social isolation, osteoporosis, and hearing disorders were identified as being associated with earlier conversion across stages. Symptomatic treatment i.e. cholinesterase inhibitors for AD was associated with later conversion from mild stage of dementia to moderate/severe stages.ConclusionThis study based on a machine learning approach allowed to identify potentially modifiable factors associated with conversion across AD stages for which timely interventions may be implemented to delay disease progression.

Cortical and subcortical gray matter abnormalities in mild cognitive impairment

Gray matter changes are thought to be closely related to cognitive decline in mild cognitive impairment (MCI) patients. The study aimed to explore cortical and subcortical structural alterations in MCI and their association with cognitive assessment. 24 MCI patients and 22 normal controls (NCs) were included. Voxel-based morphometry (VBM), vertex-based shape analysis and surface-based morphometry (SBM) analysis were applied to explore subcortical nuclei volume, shape and cortical morphology. Correlations between structural changes and cognition were explored using spearman correlation analysis. Support vector machine (SVM) classification evaluated MCI identification accuracy. MCI patients showed significant atrophy in the left thalamus, left hippocampus, left amygdala, right pallidum, right hippocampus, along with inward deformation in the left amygdala. SBM analysis revealed that MCI group exhibited shallower sulci depth in the left hemisphere and increased cortical gyrification index (GI) in the right frontal gyrus. Correlation analysis showed the positive correlation between right hippocampus volume and episodic memory, while negative correlation between the altered GI and memory performance in MCI group. SVM analysis demonstrated superior performance of sulci depth and GI derived from SBM in MCI identification. When combined with cortical and subcortical metrics, SVM achieved a peak accuracy of 89 % in distinguishing MCI from NC. The study reveals significant gray matter structural changes in MCI, suggesting their potential role in underlying functional differences and neural mechanisms behind memory impairment in MCI.

A study on the impact of acute exercise on cognitive function in Alzheimer's disease or mild cognitive impairment patients: A narrative review

This narrative review follows the JBI approach and comprehensively explores the effects and mechanisms of acute exercise on cognitive function in Alzheimer's disease (AD) and Mild cognitive impairment (MCI) patients. The results showed that the combination of acute exercise and cognitive training improved the cognitive function of AD patients better than aerobic exercise or resistance training alone. For patients with MCI, moderate intensity acute aerobic exercise and resistance exercise were beneficial to enhance Inhibitory control (IC), but high-intensity acute exercise was adverse to improve IC; Brain-derived neurotrophic factor (BDNF) and Insulin-like growth factor 1 (IGF-1) may assume the potential mediating mechanism of acute exercise on cognitive function in AD and MCI patients, but more research is needed to further confirm this mechanism.

Cognitive Profile of Patients with Borderline Personality Disorder

Background: the relevance of this study stems from the difficulties in diagnosing borderline personality disorder (BPD) and the importance of studying neurocognitive functioning for expanding the understanding of mental disorders. The available data on the cognitive profile of patients with BPD vary markedly. We could not find any studies in this area in a domestic sample. The aim of the study was to investigate the cognitive profile of patients with BPD. Patients and methods: 50 patients (72% women; n = 36; 28% men; n = 14) aged 22.4 ± 4.3 years with ICD-10 diagnosis F60.31 “Emotionally unstable personality disorder, borderline type” were examined. The research methods included clinical and scale assessment: Hospital Anxiety and Depression Scale, Hamilton Depression Scale, Hamilton Anxiety Scale, SCL-90 symptom questionnaire, Borderline Personality Disorder Questionnaire, Brief Assessment of Cognition in Schizophrenia. Results: the obtained data indicate the presence of cognitive impairment in patients with BPD. The structure of neurocognitive deficit includes impairments of working and verbal memory and attention. The severity of BPD is associated with lower cognitive functioning. No correlation between affective symptomatology in BPD and the degree of cognitive impairment was found.

Risk of Stroke, Dementia, and Cognitive Decline with Coronary and Arterial Calcification.

Extant research shows that following a cerebrovascular insult to the brain, patients may develop a wide range of cognitive disorders, spanning from mild cognitive impairment (CI) to advanced dementia. Several studies have shown that atherosclerosis in the carotid, coronary, and breast arteries is associated with an increased risk of stroke, CI, and dementia. In this review, we examine the association of subclinical atherosclerotic calcification detected by computed tomography (CT) in these arterial beds and the risk of stroke, CI, and dementia. A major advantage of CT is that it can accurately quantify vascular calcification in different parts of the vasculature during a single examination. However, the strength of the association between CT findings and CI and stroke varies with the location and severity of the arteries involved. Data are still limited on this topic, highlighting the need for additional investigations to further our understanding of the risk of cognitive impairment in patients with subclinical atherosclerosis. It is equally important to test preventive strategies for managing patients in whom vascular calcifications are identified incidentally in randomized controlled trials to study the effects on outcomes, including incidents of stroke and CI.

The Effect of Insomnia on Mild Cognitive Impairment in Patients with Cardiovascular Risk Factors: Results of a Three-Year Longitudinal Study

The Effect of Insomnia on Mild Cognitive Impairment in Patients with Cardiovascular Risk Factors: Results of a Three-Year Longitudinal Study

Alpha-lipoic acid alleviates cognitive deficits in transgenic APP23/PS45 mice through a mitophagy-mediated increase in ADAM10 α-secretase cleavage of APP

BackgroundAlpha-lipoic acid (ALA) has a neuroprotective effect on neurodegenerative diseases. In the clinic, ALA can improve cognitive impairments in patients with Alzheimer’s disease (AD) and other dementias. Animal studies have confirmed the anti-amyloidosis effect of ALA, but its underlying mechanism remains unclear. In particular, the role of ALA in amyloid-β precursor protein (APP) metabolism has not been fully elucidated.ObjectiveTo investigate whether ALA can reduce the amyloidogenic effect of APP in a transgenic mouse model of AD, and to study the mechanism underlying this effect.MethodsALA was infused into 2-month-old APP23/PS45 transgenic mice for 4 consecutive months and their cognitive function and AD-like pathology were then evaluated. An ALA drug concentration gradient was applied to 20E2 cells in vitro to evaluate its effect on the expression of APP proteolytic enzymes and metabolites. The mechanism by which ALA affects APP processing was studied using GI254023X, an inhibitor of A Disintegrin and Metalloproteinase 10 (ADAM10), as well as the mitochondrial toxic drug carbonyl cyanide m-chlorophenylhydrazone (CCCP).ResultsAdministration of ALA ameliorated amyloid plaque neuropathology in the brain tissue of APP23/PS45 mice and reduced learning and memory impairment. ALA also increased the expression of ADAM10 in 20E2 cells and the non-amyloidogenic processing of APP to produce the 83 amino acid C-terminal fragment (C83). In addition to activating autophagy, ALA also significantly promoted mitophagy. BNIP3L-knockdown reduced the mat/pro ratio of ADAM10. By using CCCP, ALA was found to regulate BNIP3L-mediated mitophagy, thereby promoting the α-cleavage of APP.ConclusionsThe enhanced α-secretase cleavage of APP by ADAM10 is the primary mechanism through which ALA ameliorates the cognitive deficits in APP23/PS45 transgenic mice. BNIP3L-mediated mitophagy contributes to the anti-amyloid properties of ALA by facilitating the maturation of ADAM10. This study provides novel experimental evidence for the treatment of AD with ALA.Graphical abstract

Clinical study of chemotherapy-related cognitive impairment in patients with non-Hodgkin lymphoma.

Chemotherapy for malignant tumors can cause brain changes and cognitive impairment, leading to chemotherapy-induced cognitive impairment (CICI). Current research on CICI has focused on breast cancer and Hodgkin's lymphoma. Whether patients with non-Hodgkin's lymphoma (NHL) undergoing chemotherapy have cognitive impairment has not been fully investigated. To investigate whether NHL patients undergoing chemotherapy had cognitive impairments. The study included 100 NHL patients who were required to complete a comprehensive psychological scale including the Brief Psychiatric Examination Scale (MMSE) at two time points: before chemotherapy and within 2 wk of two chemotherapy courses. A language proficiency test (VFT), Symbol Number Pattern Test (SDMT), Clock Drawing Test (CDT), Abbreviated Daily Cognition Scale (ECog-12), Prospective and Retrospective Memory Questionnaire, and Karnofsky Performance Status were used to assess cognitive changes before and after chemotherapy. The VFT scores for before treatment (BT) and after treatment (AT) groups were 45.20 ± 15.62, and 42.30 ± 17.53, respectively (t -2.16, P < 0.05). The CDT scores were 8 (3.5-9.25) for BT and 7 (2.5-9) for AT groups (Z -2.1, P < 0.05). Retrospective memory scores were 13.5 (9-17) for BT and 15 (13-18) for AT (Z -3.7, P < 0.01). The prospective memory scores were 12.63 ± 3.61 for BT and 14.43 ± 4.32 for AT groups (t -4.97, P < 0.01). The ECog-12 scores were 1.71 (1.25-2.08) for BT and 1.79 (1.42-2.08) for AT groups (Z -2.84, P < 0.01). The SDMT and MMSE values did not show a significant difference between BT and AT groups. Compared to the AT group, the BT group showed impaired language, memory, and subjective cognition, but objective cognition and execution were not significantly affected.

Dipsacoside B ameliorates cognitive impairment in sepsis-associated encephalopathy by reducing Th17 cell infiltration and neuroinflammation

Sepsis-associated encephalopathy (SAE) is the main cause of cognitive impairment in patients with sepsis. The infiltration of inflammatory signals into the central nervous system (CNS) via the compromised blood–brain barrier (BBB) represents a crucial step in the pathological progression of SAE. In particular, T-helper 17 cell (Th17 cells) has been suggested to be highly correlated with the activation of central immune responses. Thus, preventing Th17 cell infiltration into the CNS may be a possible strategy to alleviate cognitive decline in SAE. Dipsacoside B (DB) is one of the primary active components in Chuan Xu Duan (Dipsacus asper Wall). We speculate that DB may be a potential candidate for the treatment of SAE-related cognitive deficits. In the present study, we demonstrated that DB could effectively alleviate cognitive impairment in SAE mice. DB significantly suppressed the central inflammatory response induced by repeated lipopolysaccharide (LPS) injection. The mechanism underlying its therapeutic effect should be attributed to the reduction of BBB impairment and pathogenic Th17 cell infiltration into the CNS by inhibition of vascular endothelial growth factor A (VEGFA)/ Vascular endothelial growth factor receptor 2(VEGFR2)/ Endothelial nitric oxide synthase (eNOS) signaling. Our findings suggest that DB is a potential candidate for the treatment of SAE-related cognitive dysfunction.

Predictors of cognitive impairment in patients with substance use disorder in Kiambu County, Kenya

Predictors of cognitive impairment in patients with substance use disorder in Kiambu County, Kenya

Relationship between serum levels of folic acid and homocysteine with cognitive impairment in patients diagnosed with multiple sclerosis.

Multiple Sclerosis (MS), one of the most common neurological diseases, plays a major role in the ailments of adults. Studies on the role of homocysteine (Hcy) and folic acid in causing cognitive disorders in patients diagnosed with MS are still ongoing. This study aimed to evaluate the serum levels of folic acid and Hcy related to cognitive impairment in patients with multiple sclerosis. This prospective clinical study was conducted on 57 patients diagnosed with MS who were referred to Firoozgar Hospital, Tehran, Iran (Between November 2019 and September 2021). Demographic information and clinical characteristics of enrolled patients were recorded in a predesigned checklist. These characteristics were comprised of outcomes related to the Brief International Cognitive Assessment for MS, and the patient's Hcy and acid folic levels. Data were analyzed using SPSS version 25. Out of 57 enrolled patients, 39 subjects (68.4%) were female and 18 subjects (31.6%) were male, with a mean age of 36.87 ± 9.40 years old. In terms of disease time span, there was a mean duration of 3.80 ± 4.94 years (range: 1-23 years). There were no significant differences between the mean score of Brief International Cognitive Assessment for MS scale with patient's sex (P value: .88), and disease duration of patients (P value: .86). There was no significant relationship between the serum levels of acid folic and Hcy with cognitive impairment (P value > .05). The study results revealed that there were no significant relationships between the folic acid, Hcy levels, disease duration, and the type of MS disease with the severity of cognitive impairment. More randomized controlled clinical trials are needed to confirm the relationships between the folic acid and Hcy levels with cognitive impairment in patients with MS.

Cognitive impairment in major depressive disorder with non-suicidal self-injury: Association with the functional connectivity of frontotemporal cortex

BackgroundNon-suicidal self-injury (NSSI) may be related to serious cognitive impairment in patients with major depressive disorder (MDD), but the specific mechanism is still unclear. This study attempts to identify the neurobiological process alterations of cognitive impairment in MDD patients with NSSI by examining the functional connectivity of the frontotemporal cortex in MDD patients with or without NSSI. MethodThirty MDD patients with NSSI, 36 MDD patients without NSSI, and 35 healthy controls (HC) were included in the study. The MATRICS Consensus Cognitive Battery (MCCB) was used to comprehensively assess the cognitive function of the subjects and functional near-infrared spectroscopy (fNIRS) was used to detect the functional connectivity of the frontotemporal cortex and its brain regions of interest. ResultsMDD patients with or without NSSI had multi-domain cognitive impairments. MDD patients with NSSI showed the lowest score in performance of attention/alertness and the weakest functional connectivity of frontotemporal when compared with the MDD patients without NSSI and the HC. In addition, the functional connectivity of the bilateral frontotemporal cortex was positively correlated with verbal learning and working memory in MDD patients with NSSI. ConclusionIn MDD patients, the appearance of NSSI is often accompanied by further impairment of attention/alertness and a decline in functional connectivity of the frontotemporal cortex. The impairment of verbal learning and working memory was associated with decreased functional connectivity of the frontotemporal cortex in MDD patients with NSSI.

Abnormal white matter integrity of anterior-inferior hypothalamus in mild cognitive impairment patients with depression symptoms

BackgroundThe hypothalamus is a key brain structure involved in the pathogenesis of depression, and its abnormal activity is considered an important pathological mechanism for the formation of depression. The presence of abnormalities in the white matter integrity of hypothalamic subregions in mild cognitive impairment with depressive symptoms (D-MCI) remains unknown. MethodsIn this study, we used diffusion tensor imaging (DTI) to explore the white matter integrity of hypothalamic subregions in D-MCI. On a 3 T magnetic resonance imaging scanner, we collected DTI data from 63 subjects. The subjects included 20 healthy controls (HC), 23 MCI patients without depression (nD-MCI), and 20 patients with D-MCI. The differences in DTI metrics of hypothalamic subregions of the three groups were compared using analysis of variance and post hoc t-tests. We looked at the relationship between clinical variables and DTI metrics in hypothalamus subregions using Pearson correlation analysis. ResultsCompared with nD-MCI and HC groups, D-MCI group showed increased fractional anisotropy (FA) in anterior-inferior hypothalamus. There was a weak negative correlation between FA values in the anterior-inferior hypothalamus and depression scores in D-MCI patients. ConclusionsOur findings suggest that depressive symptoms in MCI patients are associated with abnormal white matter integrity in the anterior-inferior hypothalamus.

A nomogram for individualized prediction of mild cognitive impairment in patients with subjective cognitive decline during physical examinations: a cross-sectional study.

To develop a nomogram for mild cognitive impairment (MCI) in patients with subjective cognitive decline (SCD) undergoing physical examinations in China. We enrolled 370 patients undergoing physical examinations at the Medical Center of the First Hospital of Jilin University, Jilin Province, China, from October 2022 to March 2023. Of the participants, 256 were placed in the SCD group, and 74 were placed in the MCI group. The population was randomly divided into a training set and a validation set at a 7:3 ratio. A least absolute shrinkage and selection operator (LASSO) regression model was applied to optimize feature selection for the model. Multivariable logistic regression analysis was applied to construct a predictive model. The performance and clinical utility of the nomogram were determined using Harrell's concordance index, calibration curves, and decision curve analysis (DCA). Cognitive reserve (CR), age, and a family history of hypertension were associated with the occurrence of MCI. The predictive nomogram showed satisfactory performance, with a concordance index of 0.755 (95% CI: 0.681-0.830) in internal verification. The Hosmer-Lemeshow test results suggested that the model exhibited good fit (p = 0.824). In addition, DCA demonstrated that the predictive nomogram had a good clinical net benefit. We developed a simple nomogram that could help secondary preventive health care workers to identify elderly individuals with SCD at high risk of MCI during physical examinations to enable early intervention.

Distinguishable neural circuit mechanisms associated with the clinical efficacy of rTMS in aMCI patients.

Repetitive transcranial magnetic stimulation is used in early-stage Alzheimer's disease to slow progression, but heterogeneity in response results in different treatment outcomes. The mechanisms underlying this heterogeneity are unclear. This study used resting-state neuroimaging to investigate the variability in episodic memory improvement from angular gyrus repetitive transcranial magnetic stimulation and tracked the neural circuits involved. Thirty-four amnestic mild cognitive impairment patients underwent angular gyrus repetitive transcranial magnetic stimulation (4weeks, 20Hz, 100% resting motor threshold) and were divided into high-response and low-response groups based on minimal clinically important differences in auditory verbal learning test scores. Baseline and pre/post-treatment neural circuit activities were compared. Results indicated that the orbital middle frontal gyrus in the orbitofrontal cortex network and the precuneus in the default mode network had higher local activity in the low-response group. After treatment, changes in local and remote connectivity within brain regions of the orbitofrontal cortex, default mode network, visual network, and sensorimotor network showed opposite trends and were related to treatment effects. This suggests that the activity states of brain regions within the orbitofrontal cortex and default mode network could serve as imaging markers for early cognitive compensation in amnestic mild cognitive impairment patients and predict the aftereffects of repetitive transcranial magnetic stimulation response.

Long-Term Visit-to-Visit Blood Pressure Variability and Cognitive Decline Among Patients With Hypertension: A Pooled Analysis of 3 National Prospective Cohorts.

A limited number of studies investigated the association between blood pressure variability (BPV) and cognitive impairment in patients with hypertension. This study aimed to identify the longitudinal association between BPV and cognitive decline and the role of blood pressure (BP) control in this association. Participants with hypertension from the HRS (Health and Retirement Study), the ELSA (English Longitudinal Study of Ageing), and the CHARLS (China Health and Retirement Longitudinal Study) were included. Variation independent of the mean (VIM) was adopted to measure BPV. Cognitive function was measured by standard questionnaires, and a standardized Z score was calculated. Linear mixed-model and restricted cubic splines were adopted to explore the association between BPV and cognitive decline. The study included 4853, 1616, and 1432 eligible patients with hypertension from the HRS, ELSA, and CHARLS, respectively. After adjusting for covariates, per-SD increment of VIM of BP was significantly associated with global cognitive function decline in Z scores in both systolic BP (pooled β, -0.045 [95% CI, -0.065 to -0.029]) and diastolic BP (pooled β, -0.022 [95% CI, -0.040 to -0.004]) among hypertensive patients. Similar inverse associations were observed in patients with hypertension taking antihypertensive drugs and in patients with hypertension with well-controlled BP. High BPV was independently associated with a faster cognitive decline among patients with hypertension, even those with antihypertensive medications or well-controlled BP. Further studies are needed to confirm our results and determine whether reducing BPV can prevent or delay cognitive decline.

Factors associated with cancer-related cognitive impairment in patients with lung cancer: A systematic review

PurposeCognitive impairment is common in lung cancer patients and impacts their quality of life. Little is known about the etiology of cognitive impairment in lung cancer patients. However, the associated factors of cognitive impairment among lung cancer patients have not been systematically reviewed. This review aimed to summarize the factors related to cognitive impairment among lung cancer patients. MethodsPubMed, EMBASE, PsycINFO, CINAHL Plus, and Web of Science were searched to retrieve articles published from data inception until January 21, 2024, focusing on factors associated with cognitive impairment among lung cancer patients. Critical appraisal was undertaken by two reviewers independently using the Newcastle–Ottawa Scale. ResultsA total of 17 observational studies were included. The results showed that 20 factors are associated with cognitive impairment, including psychological factors (loneliness, fatigue, anxiety, depression, high symptom burden, and baseline cognitive impairment), lifestyle and functional factors (daily step counts, smoking, and activities of daily living or instrumental activities of daily living impairments), medical treatment factors (cranial irradiation, chemotherapy, lobar resection, postoperative delirium, and on medication), and neuroimmunological factors (have neuronal autoantibodies, altered Default Mode Network connectivity, dysregulation in glutamate and glutamate metabolism, mitochondrial dysfunction, blood-brain barrier leakage, and reduced T-lymphocytes). ConclusionThis is the first study to systematically review 20 factors associated with cognitive impairment among lung cancer patients, encompassing psychology, lifestyle and functional, medical treatment, and neuroimmunological factors. These findings can help clinicians identify at-risk patients and develop evidence-based interventions to prevent cognitive impairment among lung cancer patients.

Terapia psicológica grupal y su efecto en ansiedad, depresión y niveles de BDNF en candidatos a trasplante renal

The objective of the present study is to describe the effect of a group intervention on the levels of anxiety and depression associated with the level of BDNF and cognitive impairment of patients who are candidates for kidney transplantationthrough a pre-experimental study. 25 adult patients of both gendersof a High Specialty Medical Unitparticipated in the study. The Beck depression and Golberg anxiety inventories and the Folstein Mini Mental State Exam were applied. At the beginning and end of the intervention, blood and urine samples were taken to analyze BDNF levels. A group intervention with a brief orientation cognitive behavioral approach was carried out. The results in the variables of anxiety (p = 0.002) and depression (p = 0.04) show significant differences before and after the interventionreducing the levels of these variables considerably; Regarding BDNF levels and cognitive impairment, no significant differences were found.This study shows the usefulness of group psychological therapies for the benefit of these patients as well as the need to carry out more studies that evaluate biological markers related to the pathologies presented.

Increased Blood-Brain Barrier Permeability and Cognitive Impairment in Patients With ESKD

Background and AimsChronic kidney disease (CKD) is associated with an increased risk of cognitive impairment. This cognitive impairment is associated with an increased permeability of blood-brain barrier (BBB) in rodents with CKD, linked to activation of aryl hydrocarbon receptor (AhR) by indoxyl sulphate (IS). The objective of BREIN study is to confirm the increased BBB permeability in humans with CKD. MethodThe BREIN comparative study (NCT04328415) prospectively included patients with end-stage kidney disease (ESKD), and healthy volunteers (Ctrl) matched in age, sex, and educational level to a patient. In all participants, BBB permeability was quantified by brain 99mTc-DTPA SPECT/CT as percentage of injected activity (%IA). A battery of neuro-cognitive tests was performed, serum uremic toxins accumulation and AhR activation were assessed. ResultsFifteen ESKD patients and 14 healthy volunteers were analysed. ESKD patients had higher BBB permeability compared to controls: 0.29±0.07 vs. 0.14±0.06 %IA, p=0.002. ESKD patients displayed lower MoCA score: 22.0±5.0 vs. 27.3 ± 2.8, p=0.008, impaired short-term memory (doors test): 12.5±3.4 vs. 16.5±3.4, p=0.005, higher Beck depression score 8.1±9.1 vs. 2.7±3.4, p=0.046, and slightly more daily cognitive complaints: 42.5±29.3 vs. 29.8±14.0 p=0.060. ESKD patients displayed higher IS levels (86.1±48.4 vs. 3.2±1.7 μmol/L, p=0.001) and AhR activating potential (37.7±17.8% vs. 24.7±10.4%, p=0.027). BBB permeability was inversely correlated with MoCA score (r=-0.60, 95%CI [-0.772; -0.339], p=0.001) in the overall population. ConclusionESKD patients display an increased BBB permeability compared to matched healthy volunteers. Association with uremic toxins and cognitive impairment needs to be assessed in larger cohorts of patients.