Correlation of common inflammatory cytokines with cognition impairment, anxiety, and depression in acute ischemic stroke patients

Abstract

Inflammatory cytokines are related to cognitive function and psychiatric disorders in patients with several diseases. However, few relevant studies have been performed on acute ischemic stroke (AIS) patients. Hence, this study aimed to investigate the correlation of common inflammatory cytokines with cognition impairment, anxiety, and depression in AIS patients. Common inflammatory cytokines of 176 AIS patients (including tumor necrosis factor-alpha (TNF-a), interleukin (IL)-1b, IL-6, and IL-17) were measured using Human Enzyme Linked Immunosorbent Assay Kits. Cognition impairment (Mini-Mental State Examination (MMSE)), anxiety (Hospital Anxiety and Depression Scale for anxiety (HADS-A)), and depression (HADS-D) were evaluated. The incidence of cognition impairment, anxiety, and depression was 43.2, 39.2, and 31.2%, respectively. TNF-a and IL-6 were negatively associated with MMSE score, and high TNF-a, IL-1b, and IL-6 were correlated with cognition impairment occurrence. In addition, TNF-a, IL-1b, and IL-17 were positively associated with HADS-A score, while only high TNF-a was associated with anxiety occurrence. Furthermore, TNF-a, IL-1b, and IL-17 were positively associated with HADS-D score, while high IL-1b, IL-6, and IL-17 correlated with depression occurrence. Multivariate logistic regression revealed that TNF-a and National Institutes of Health Stroke Scale (NIHSS) score X5 were associated with high risk of cognition impairment; TNF-a, IL-17, unemployed before surgery, hypertension, and chronic kidney disease (CKD) correlated with high anxiety occurrence. Furthermore, IL-17, divorced/widowed/single status, diabetes, and NIHSS score X5 were associated with high risk of depression. In conclusion, common inflammatory cytokines including TNF-a, IL-1b, and IL-17 were related to cognition impairment, anxiety, or depression in AIS patients.

The longitudinal changes of serum JKAP and IL‐17A, and their linkage with anxiety, depression, and cognitive impairment in acute ischemic stroke patients

“…It was discovered that the incidence of anxiety, depression, and cognitive impairment were 33.3%, 29.2%, and 25.0%, respectively, which was partly in line with a previous study (anxiety: 39.2%; depression: 31.2%; cognitive impairment: 43.2%). 21 This finding indicated that anxiety, depression, and cognitive impairment were critical issues in AIS patients.…”

“… 18 In terms of IL‐17A, it is positively linked with anxiety, depression, and cognitive impairment in AIS patients. 21 Importantly, our recently published study discovers that JKAP is reduced, and negatively related to the National Institutes of Health Stroke Scale (NIHSS) score in AIS patients 17 ; however, the intercorrelation between JKAP and IL‐17A, and their clinical role in estimating psychological health in AIS patients should be further explored.…”

“… 13 , 14 , 15 , 16 Besides, a few studies also report the linkage of JKAP and IL‐17A with mental health in inflammation‐mediated and neurological disease patients. 13 , 17 , 18 , 19 , 20 , 21 For instance, JKAP is reversely linked with cognitive impairment progression in Alzheimer's disease patients. 18 In terms of IL‐17A, it is positively linked with anxiety, depression, and cognitive impairment in AIS patients.…”

“…Jun N‐terminal kinase (JNK) pathway‐associated phosphatase (JKAP), as a key JNK regulator, inactivates T‐cell receptor (TCR) signaling to involve in T‐cell mediated immunity, and suppresses Lck to reduce the secretion of interleukin (IL)‐17A, thereby participating in the pathology and progression of neurological diseases 13–16 . Besides, a few studies also report the linkage of JKAP and IL‐17A with mental health in inflammation‐mediated and neurological disease patients 13,17–21 . For instance, JKAP is reversely linked with cognitive impairment progression in Alzheimer's disease patients 18 .…”

Effects of gestational inflammation on age-related cognitive decline and hippocampal Gdnf-GFRα1 levels in F1 and F2 generations of CD-1 Mice

“…IL-1β, IL-6 and TNF-α are the most common pro-inflammatory cytokines; in inflammatory states (such as LPS challenge), these factors amplify their own production via autocrine induction and interact with other inflammatory mediators. A large body of literature indicates that over-expression of IL-1β, IL-6 and TNF-α has a detrimental effect on cognitive function [26][27][28][29] by affecting synaptic plasticity, longterm potentiation, neurogenesis, and brain structures (especially hippocampal regions) [30][31][32][33]. However, it remains unclear whether maternal gestational inflammation leads to altered GDNF levels and promotes AACD in direct (F1) and subsequent (F2) offspring.…”