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BACKGROUND: Frailty is proposed as a predictor of outcomes in patients undergoing major surgeries, although data on the association of frailty and coronary artery bypass grafting (CABG) are lacking. We assessed the association between frailty and cognitive and clinical complications following CABG. METHODS: This prospective study included patients aged over 60 years undergoing elective CABG at Tehran Heart Center from 2020 to 2022. Baseline and three-month follow-up data on frailty using the Frail scale and clinical Frail scale, functional status using the Lawton Instrumental Activities of Daily Living Scale (IADL), cognitive function by Montreal Cognitive Assessment (MoCA), and depression by the Geriatric Depression Scale (GDS) were obtained. The incidence of adverse outcomes was investigated at the three-month follow-up. Outcomes between frail and non-frail groups were compared utilizing T-tests and Mann-Whitney U tests, as appropriate. RESULTS: We included 170 patients with a median age of 66 ± 4 years (75.3% male). Of these, 58 cases were classified as frail, and 112 individuals were non-frail, preoperatively. Frail patients demonstrated significantly worse baseline MOCA scores (21.08 vs. 22.41, P = 0.045), GDS (2.00 vs. 1.00, P = 0.009), and Lawton IADL (8.00 vs. 6.00, P < 0.001) compared to non-frail. According to 3-month follow-up data, postoperative MOCA and GDS scores were comparable between the two groups, while Lawton IADL (8.00 vs. 6.00, P < 0.001) was significantly lower in frail cases. A significantly higher rate of readmission (1.8% vs. 12.1%), sepsis (7.1% vs. 19.0%), as well as a higher Euroscore (1.5 vs. 1.9), was observed in the frail group. A mildly significantly more extended ICU stay (6.00 vs. 5.00, p = 0.051) was shown in the frail patient. CONCLUSION: Frailty showed a significant association with a worse preoperative independence level, cognitive function, and depression status, as well as increased postoperative complications.
Subject(s)
Frailty , Aged , Humans , Male , Middle Aged , Female , Frailty/diagnosis , Prospective Studies , Frail Elderly , Activities of Daily Living , Geriatric Assessment , Iran/epidemiology , Coronary Artery Bypass/adverse effects , Postoperative Complications/diagnosis , Postoperative Complications/epidemiology , Postoperative Complications/etiology , CognitionABSTRACT
BACKGROUND: The blood biomarker neurofilament light (NFL) is one of the most widely used for monitoring Alzheimer's disease (AD). According to recent research, a higher NFL plasma level has a substantial predictive value for cognitive deterioration in AD patients. Diffusion tensor imaging (DTI) is an MRI-based approach for detecting neurodegeneration, white matter (WM) disruption, and synaptic damage. There have been few studies on the relationship between plasma NFL and WM microstructure integrity. AIMS: The goal of the current study is to assess the associations between plasma levels of NFL, CSF total tau, phosphorylated tau181 (P-tau181), and amyloid-ß (Aß) with WM microstructural alterations. METHODS: We herein have investigated the cross-sectional association between plasma levels of NFL and WM microstructural alterations as evaluated by DTI in 92 patients with mild cognitive impairment (MCI) provided by Alzheimer's Disease Neuroimaging Initiative (ADNI) participants. We analyzed the potential association between plasma NFL levels and radial diffusivity (RD), axial diffusivity (AxD), mean diffusivity (MD), and fractional anisotropy (FA) in each region of the Montreal Neurological Institute and Hospital (MNI) atlas, using simple linear regression models stratified by age, sex, and APOE ε4 genotype. RESULTS: Our findings demonstrated a significant association between plasma NFL levels and disrupted WM microstructure across the brain. In distinct areas, plasma NFL has a negative association with FA in the fornix, fronto-occipital fasciculus, corpus callosum, uncinate fasciculus, internal capsule, and corona radiata and a positive association with RD, AxD, and MD values in sagittal stratum, corpus callosum, fronto-occipital fasciculus, corona radiata, internal capsule, thalamic radiation, hippocampal cingulum, fornix, and cingulum. Lower FA and higher RD, AxD, and MD values are related to demyelination and degeneration in WM. CONCLUSION: Our findings revealed that the level of NFL in the blood is linked to WM alterations in MCI patients. Plasma NFL has the potential to be a biomarker for microstructural alterations. However, further longitudinal studies are necessary to validate the predictive role of plasma NFL in cognitive decline.
Subject(s)
Alzheimer Disease , White Matter , Humans , White Matter/diagnostic imaging , Alzheimer Disease/diagnostic imaging , Diffusion Tensor Imaging/methods , Cross-Sectional Studies , Intermediate Filaments , Brain/diagnostic imaging , BiomarkersABSTRACT
Alzheimer's disease (AD) is a progressive neurodegenerative disease associated with dementia and is a serious concern for the health of individuals and government health care systems worldwide. Gray matter atrophy and white matter damage are major contributors to cognitive deficits in AD patients, as demonstrated by magnetic resonance imaging (MRI). Many of these brain changes associated with AD begin to occur about 15 years before the onset of initial clinical symptoms. Therefore, it is critical to find biomarkers reflective of these brain changes associated with AD to identify this disease and monitor its prognosis and development. The increased plasma level of hyperphosphorylated tau 181 (p-tau181) has been recently considered a novel biomarker for the diagnosis of AD, preclinical AD, and mild cognitive impairment (MCI). In the current study, we examined the association of cerebrospinal fluid (CSF) and plasma levels of p-tau181 with structural brain changes in cortical thickness, cortical volume, surface area, and subcortical volume in MCI patients. In this cross-sectional study, we included the information of 461 MCI patients from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort. The results of voxel-wise partial correlation analyses showed a significant negative correlation between the increased levels of plasma p-tau181, CSF total tau, and CSF p-tau181 with structural changes in widespread brain regions. These results provide evidence for the use of plasma p-tau181 as a diagnostic marker for structural changes in the brain associated with the early stages of AD and neurodegeneration.
Subject(s)
Alzheimer Disease , Cognitive Dysfunction , tau Proteins , Aged , Alzheimer Disease/blood , Alzheimer Disease/complications , Biomarkers/blood , Cognitive Dysfunction/diagnosis , Cognitive Dysfunction/etiology , Cross-Sectional Studies , Female , Humans , tau Proteins/bloodABSTRACT
Background: Several different endovascular and non-invasive treatment methods are suggested for the various types of intracranial aneurysms including simple, balloon-assisted, and stent-assisted coiling (SAC). Previous studies investigated the safety and efficacy of SAC versus non-stent-assisted coiling (non-SAC) but the results were controversial. We aim to perform a systematic review and meta-analysis to compare the efficacy and safety of SAC with non-SAC technique in stratifying by the ruptured and unruptured aneurysms. Methods: PubMed, Scopus, Web of Science, and Cochrane Central Register of Controlled Trials were searched in April 2022 for studies investigated the efficacy and safety of SAC versus non-SAC. Results: Overall, 26 studies entered into our qualitative and quantitative synthesis. We found that there was overall lower recurrence rate in SAC versus non-SAC significant (RR: 0.43, 95%CI: 0.33, 0.53). Furthermore, the comparisons were significant in unruptured (RR: 0.63, 95%CI: 0.40, 0.86), ruptured (RR: 0.29, 95%CI), and combination aneurysms (RR: 0.42, 95%CI: 0.30, 0.54). Also, we found higher risk of intraprocedural rupture for SAC versus non-SAC in unruptured aneurysms (RR: 1.40, 95%CI: 1.31, 1.50). Investigating hemorrhagic events risk showed that there was significant difference in ruptured (RR: 1.73, 95%CI: 1.12, 2.34) and combination aneurysms (RR: 0.60, 95%CI: 0.37, 0.82). There was no significant difference in immediate occlusion rate, complete occlusion, and risk of ischemic events in our analysis. Conclusion: Overall, our findings demonstrated that SAC may have higher efficacy in term of recurrence rate, but also may have a higher risk of complications in the treatment of intracranial aneurysms. As there are several factors affecting the outcomes and safety of these interventions, further RCTs controlled for multiple factors are required better guide the neurointerventionists choose the best strategy.
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BACKGROUND: There are contradictory findings regarding the effect of statin drugs on amyloid ß (Aß) deposition as one of the main hallmarks of Alzheimer's disease (AD), along with tau pathology. We aimed to longitudinally investigate the therapeutic and preventive role of statin drugs by examining the brain Aß deposition and metabolism rate in AD, mild cognitive impairment (MCI), and healthy controls (HC). METHODS: The data of 828 subjects including 178 HC, 492 MCI, and 158 AD individuals were obtained from ADNI. The baseline and longitudinal [18 F] AV45 and 18-fluorodeoxyglucose (FDG) PET standard uptake value ratio (SUVR) measures were investigated among statin users and non-users. RESULTS: Our results showed that there is no significant difference in baseline Aß deposition and metabolism rate between statin users and non-users among HC, MCI, and AD subjects. While there was no significant effect of statin on metabolism rate, there was a significant difference in Aß deposition change after 4 years (from baseline) between statin users and non-users within HC subjects (p = 0.011). The change of Aß deposition at 4 years from baseline was -2.0 ± 6.3% for statin users and 1.4 ± 4.7% for non-users. There was no significant association between statin duration use with baseline and longitudinal Aß deposition and metabolism rate. However, statin dosage was significantly associated with Aß deposition in 2 years (r = -0.412, p = 0.021) in the HC group. Moreover, our analysis showed a significant correlation between total statin exposure (duration×dosage) and Aß deposition in 2 years visit (r = -0.198, p = 0.037) in HC subjects. Furthermore, we investigated the longitudinal changes within each group of statin users and non-users separately in linear mixed models. Our findings showed that there are no significant changes in AV45 and FDG SUVR among both groups. CONCLUSION: The present longitudinal analysis revealed that using statins might be beneficial in slowing down or stabilizing the Aß deposition due to aging in subjects without cognitive impairment. However, once the clinical symptoms of cognitive impairment appear, statins fail to slow down Aß deposition. Overall, our findings revealed that statin users might have slower Aß aggregation than non-users.
Subject(s)
Alzheimer Disease , Cognitive Dysfunction , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Humans , Amyloid beta-Peptides/metabolism , Hydroxymethylglutaryl-CoA Reductase Inhibitors/therapeutic use , Fluorodeoxyglucose F18 , Alzheimer Disease/diagnostic imaging , Alzheimer Disease/drug therapy , Alzheimer Disease/metabolism , Cognitive Dysfunction/diagnostic imaging , Cognitive Dysfunction/drug therapy , Cognitive Dysfunction/metabolism , Brain/metabolism , Positron-Emission Tomography/methodsABSTRACT
BACKGROUND: Association between traumatic brain injury (TBI) and Parkinson's disease (PD) has been a hot topic of discussion for a long time. Previous studies reported that the incidence of PD is significantly higher among elderly adults with a history of TBI. Due to contradictory results of previous investigations, we aimed to perform a systematic review and meta-analysis to investigate the role of TBI as a risk factor for PD. METHODS: We conducted a systematic literature search in the electronic databases PubMed, Web of Science, and Scopus. In this study, we included published papers on the risk of PD in patients with previous TBI compared to the healthy control group. RESULTS: After the screening, 15 studies entered our systematic review and meta-analysis. The risk ratio of TBI among PD and controls by a combination of 15 studies using a random-effect model was 1.48 (95% CI 1.22-1.74). The prevalence of TBI by a combination of 14 studies was 18% (95% CI 12-24%). CONCLUSION: Our result suggests that TBI is a major risk factor for developing PD later in life. At this time, there is a lack of populous prospective cohort studies with sufficient follow-up period to provide a well-documented association between the onset of PD and severity, frequency, and location of prior TBI, which warrants special efforts and consideration for years to come.
Subject(s)
Brain Injuries, Traumatic , Parkinson Disease , Adult , Humans , Aged , Parkinson Disease/epidemiology , Parkinson Disease/complications , Prospective Studies , Brain Injuries, Traumatic/complications , Brain Injuries, Traumatic/epidemiology , Risk Factors , IncidenceABSTRACT
Background: Risk stratification of patients for incidence of stroke and its outcomes can aid in decision-making regarding treatment options and rehabilitative care. We systematically reviewed the literature to provide comprehensive evidence for the value of serum soluble suppression of tumorigenicity-2 (sST-2) in the prediction of stroke incidence and the evaluation of post-stroke outcomes. Methods: The Medline, Scopus, Web of Science, and Embase databases were searched until the end of August 2022 for studies investigating the value of serum sST-2 in the prediction of stroke incidence and post-stroke outcomes. Results: Nineteen articles were included. The articles reported conflicting results on the predictive value of sST-2 measurement in the incidence of stroke. Studies investigating the value of sST-2 measurement for the prognosis of post-stroke outcomes have reported positive associations between sST-2 levels and post-stroke mortality, composite adverse events, major disability, cerebral-cardiac syndrome, and cognitive impairment. Conclusions: Although some studies have reported a predictive value of serum sST-2 measurement in the incidence of stroke, a clear consensus has yet to be reached because of discrepancies in the results. As for the prognosis of post-stroke outcomes, sST-2 may be a predictor of mortality, composite adverse events, and major disability after stroke. Overall, more well-designed prospective cohort studies are needed to reach a more decisive conclusion on the value of sST-2 measurement for the prediction of stroke and its outcomes and to determine optimal cutoffs.
Subject(s)
Stroke , Humans , Prognosis , Prospective Studies , Databases, Factual , Stroke/diagnosis , SyndromeABSTRACT
Background: Recent findings suggest that the plasma axonal structural protein, neurofilament light (NFL) chain, may serve as a potential blood biomarker for early signs of neurodegenerative diseases, such as Alzheimer's disease (AD). Given the need for early detection of neurodegenerative disorders, the current study investigated the associations between regional cerebral blood flow (rCBF) in brain regions associated with neurodegenerative disorders and memory function with plasma NFL in AD, mild cognitive impairment (MCI), and healthy controls (HCs). Methods: We recruited 29 AD, 76 MCI, and 39 HCs from the Alzheimer's Disease Neuroimaging Initiative (ADNI) database in the current cross-sectional study. We used Pearson's correlation models adjusted for the effect of age, sex, and APOE genotype to investigate the association between plasma NFL and rCBF. Results: We found non-significant differences in age (F(2, 141) = 1.304; P = 0.275) and years of education (F(2, 141) = 0.013; P = 0.987). Additionally, we found significant differences between groups in terms of MMSE scores (F(2, 141) = 100.953; P < 0.001). Despite the observation of significantly reduced rCBF in AD and MCI groups versus HCs, we did not detect significant differences in plasma NFL between these groups. We found significant negative associations between plasma NFL and rCBF in various AD-related regions, these findings were only observed after analyses in all participants, and were observed in HCs alone and no significant associations were observed in the AD or MCI groups. Conclusion: These outcomes add to our current understanding surrounding the use of rCBF and plasma NFL biomarkers as tools for early detection and diagnosis of neurodegenerative diseases. A conclusion might be that the association between NFL and impaired rCBF exists before the clinical symptoms appear. Further longitudinal studies with a large sample size should be performed to examine the correlation between plasma NFL and rCBF in order to understand these complex relationships.
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BACKGROUND: There were concerns about the psychological outcomes of coronavirus disease from the beginning of the pandemic. Parkinson's disease (PD) patients seem to be more vulnerable to mental health disorders like stress, depression, anxiety, or worsening quality of life during COVID-19 lockdown. We aimed to conduct a systematic review to investigate the psychological outcomes of COVID-19 among the PD population. METHODS: A systematic search was conducted using PubMed, Scopus, and Web of Science. We included original studies which reported the psychological impact of COVID-19 in the PD population with a minimum of 10 cases. RESULTS: After the screening, 21 studies with a total of 5236 PD cases were included in our qualitative synthesis. Depression, anxiety, and to less extent sleep disorders and apathy are the most studied psychological outcomes. Most of the studies indicated that the severity or the prevalence of psychiatric disturbance increased due to the COVID-19 pandemic in PD patients. The prevalence of anxiety was 14% to 66.5%, while depression was reported in 0% to 50% of PD patients during and after the pandemic. Also, sleep problems were reported in 35.4% to 68.9% of PD patients. CONCLUSION: Considering the overall trend of increment in the severity of the main psychological outcomes observed in the present systematic review, it is suggested that future studies conduct a more accurate analysis of the prevalence, severity, and associated pathology of psychological outcomes of COVID-19 in PD patients.
Subject(s)
COVID-19 , Parkinson Disease , Anxiety/epidemiology , Anxiety/etiology , Anxiety/psychology , COVID-19/epidemiology , Communicable Disease Control , Depression/epidemiology , Depression/etiology , Depression/psychology , Humans , Pandemics , Parkinson Disease/complications , Parkinson Disease/epidemiology , Parkinson Disease/psychology , Quality of Life , Stress, Psychological/epidemiologyABSTRACT
INTRODUCTION: There are increasing reports of COVID-19 related neurological complications which may be due to direct viral invasion, or immune mediated inflammatory diseases such as autoimmune encephalitis and ADEM (acute demyelinating encephalomyelitis). In this study, a systematic review is presented of the reported cases infected by the COVID-19 who were diagnosed with various forms of autoimmune encephalitis (AE). METHODS: The authors searched three databases including PubMed, Scopus, and Web of science for extracting original articles on coronavirus/ COVID-19 and AE. RESULTS: Eighteen articles were considered in this study, including 15 case reports, and three case series with a total of 81 patients. Among the studies, 19 cases were reported with AE including 7 (37%) cases of limbic encephalitis, 5 (26%) patients with anti-N-methyl-d-aspartate (NMDA) receptor encephalitis, 2 (11%) with AE presenting as new-onset refractory status epilepticus (NORSE), 1 (5%) case of steroid-responsive encephalitis, and 4 (21%) cases with an unknown type of AE. CONCLUSION: Our systematic review revealed evidence on AE development in patients infected with the COVID-19. Clinicians should be aware of the possible diagnosis of AE when considering other neurological differential diagnosis in SARS-CoV-2 infected patients.
Subject(s)
Anti-N-Methyl-D-Aspartate Receptor Encephalitis , COVID-19 , Hashimoto Disease , Anti-N-Methyl-D-Aspartate Receptor Encephalitis/diagnosis , COVID-19/complications , Encephalitis , Hashimoto Disease/complications , Hashimoto Disease/diagnosis , Humans , SARS-CoV-2ABSTRACT
OBJECTIVE: There is a shred of growing evidence demonstrating that diabetic patients are at higher risk of developing Alzheimer's disease compared to the general population. The previous investigation showed the protective effect of metformin for delaying dementia in diabetic patients. However, there are limited data on the effect of metformin on structural changes. This study aims to investigate the effect of metformin on hippocampal and cortical volumes in non-demented diabetic individuals. METHOD: We entered 157 non-demented diabetic subjects including 89 mild cognitive impairment (MCI), and 68 cognitively healthy individuals from Alzheimer's disease Neuroimaging Initiative (ADNI) which were then categorized as metformin users and non-users. We used the ANCOVA model for measuring the association between metformin use and hippocampal and cortical volumes. RESULTS: Among 157 subjects with a mean age of 71.8 (±7.7) included in this study, 76 individuals were stratified as metformin users. Results of the univariate model indicate that metformin users had a higher right (p = 0.003) and left parietal lobe volume (p = 0.004). Moreover, the volume of left cingulate was higher in those who used metformin compared to those not used it (p = 0.027). Our results were also significant for the right frontal lobe and indicated that metformin users had higher volume (p = 0.035). There were no significant differences in the hippocampus, occipital, and temporal regions. CONCLUSION: Our findings showed the protective effects of metformin on brain volumes in non-demented elderly individuals with diabetes. Comparing the groups show strong enough results regarding the lower atrophy in metformin users.
Subject(s)
Alzheimer Disease , Cognitive Dysfunction , Diabetes Mellitus , Metformin , Aged , Alzheimer Disease/pathology , Atrophy/pathology , Brain/pathology , Diabetes Mellitus/drug therapy , Hippocampus/pathology , Humans , Magnetic Resonance Imaging , Metformin/therapeutic useABSTRACT
Amyotrophic lateral sclerosis (ALS) is a paralytic, heterogeneous and progressive disease characterized by the degeneration of both upper and lower motor neurons. Several studies about the effects of statins drug on the risk of ALS showed contradictory results and evidence for this is inconclusive. So we aimed to perform a meta-analysis on previous studies to clarify the association between statin use and risk of ALS. The databases including PubMed, Scopus, and Web of science were searched in February 2021 for studies that reported the association between statin use and risk of ALS. The eligible studies had to provide a report on the effect of statin and the incidence of ALS while comparing it to the control group. Articles that had low statin exposure time, the absence of a control group and an unknown number of ALS patients were excluded. The rate ratio and 95% confidence interval (CI) were used for association measures in case-control and cohort studies. After full-text and abstract review, data from 8 studies with a total of 547,622 participants and 13,890 cases of ALS were entered in the present meta-analysis. We combined eight studies using a random-effect model and the RR for statin users among groups was 0.98 (95% CI 0.80-1.20) which indicates no association between statin and incidence of ALS. Also high heterogeneity was detected across the studies (Q value = 26.62, P = .00; I2 = 72.71%). In our meta-analysis study, we found no association between statin use and an increase in ALS incidence. This result is in line with some previous studies and provides strong evidence that denies the possible association between statin uptake and disease induction.
Subject(s)
Amyotrophic Lateral Sclerosis , Hydroxymethylglutaryl-CoA Reductase Inhibitors , Amyotrophic Lateral Sclerosis/chemically induced , Amyotrophic Lateral Sclerosis/epidemiology , Case-Control Studies , Cohort Studies , Humans , Hydroxymethylglutaryl-CoA Reductase Inhibitors/adverse effects , IncidenceABSTRACT
Background: Cognitive impairments in patients with multiple sclerosis (MS) are suggested as a prognostic factor for disease development, and consequently higher disability and more deficits in daily and social activities. In this regard, we aimed to investigate the association between quality of life (QOL) and cognitive function in patients with MS. Methods: We conducted a cross-sectional study on patients with relapsing-remitting MS (RRMS). General characteristic variables were carried out, and then all patients underwent assessments such as Multiple Sclerosis Quality of Life-54 (MSQOL-54), Minimal Assessment of Cognitive Function in Multiple Sclerosis (MACFIMS), Expanded Disability Status Scale (EDSS), Beck Depression Inventory-II (BDI-II), and North American Adult Reading Test (NAART). Results: In the present study, a total of 92 patients, including 76 women with a mean disease duration of 6.82 ± 4.80 years were involved. Results of simple Pearson correlation revealed a significant positive relation between California Verbal Learning Test (CVLT) total learning with MSQOL mental health (r = 0.267, P = 0.017) and physical health (r = 0.299, P = 0.007). After adjusting for potential confounders, there was a negative correlation between MSQOL mental health with Delis-Kaplan Executive Function System (D-KEFS) (r = -0.303, P = 0.015) and Judgment of Line Orientation (JLO) (r = -0.310, P = 0.013). Besides, MSQOL physical health was negatively associated with Brief Visuospatial Memory Test-Revised (BVMT-R) in the adjusted model (r = -0.270, P = 0.031). Conclusion: There is a statistically significant association between specific aspects of cognitive decline and QOL. Therefore, more attention should be paid to cognitive impairment in patients with MS as based on our findings, it is significantly associated with QOL.