scholarly journals Synergistic Effects of Aldehyde Dehydrogenase 2 Polymorphisms and Alcohol Consumption on Cognitive Impairment after Ischemic Stroke in Han Chinese

2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Ying Yu ◽  
Jie Gao ◽  
Shasha Wang ◽  
Heng Lv ◽  
Liping Xiao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cognitive Impairment ◽  
Alcohol Consumption ◽  
Aldehyde Dehydrogenase ◽  
Cognitive Rehabilitation ◽  
Han Chinese ◽  
Binary Logistic Regression Analysis ◽  
Aldehyde Dehydrogenase 2 ◽  
Stroke Patients ◽  
Cutoff Scores

Aldehyde dehydrogenase 2 (ALDH2) polymorphisms are related to both stroke risk and alcohol consumption. However, the influence of ALDH2 polymorphisms and alcohol consumption on cognitive impairment after ischemic stroke remains unknown, as do the possible mechanisms. We enrolled 180 Han Chinese ischemic stroke patients from four community health centers in Bengbu, China. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA), and two different MoCA cutoff scores were used to define cognitive impairment in ischemic stroke patients. The ALDH2 genotypes were determined using polymerase chain reaction and direct sequencing. To assess the associations of ALDH2 polymorphisms and alcohol consumption with cognitive impairment after ischemic stroke, we performed binary logistic regression analysis with odds ratios. We revealed that individuals with the ALDH2 wild-type genotype were more likely to have high MoCA scores than those with the mutant and heterozygous types ( p = 0.034 ). In addition, using two MoCA cutoff scores, the percentage of moderate to excessive alcohol consumption in the cognitive impairment group was higher than that in the nonimpairment group ( p = 0.001 ). The levels of 4-hydroxy-2-nonenal ( p = 0.001 ) and swallowing function ( p = 0.001 ) were also higher in the cognitive impairment group than in the nonimpairment group. Moreover, after adjusting for other potential risk factors, ALDH2 polymorphisms and alcohol consumption had a significant synergistic effect on cognitive impairment ( p = 0.022 ). Specifically, the ALDH2 ∗ 2 mutant allele and higher alcohol consumption were associated with cognitive impairment and swallowing ability after ischemic stroke. Targeting ALDH2 may be a useful biomarker for cognitive rehabilitation following ischemic stroke.

scholarly journals Association of ADH1B polymorphism and alcohol consumption with increased risk of intracerebral hemorrhagic stroke

2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Chun-Hsiang Lin ◽  
Oswald Ndi Nfor ◽  
Chien-Chang Ho ◽  
Shu-Yi Hsu ◽  
Disline Manli Tantoh ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Alcohol Consumption ◽  
Genetic Variants ◽  
Regression Models ◽  
Hemorrhagic Stroke ◽  
Alcohol Exposure ◽  
Modifiable Risk Factors ◽  
Aldehyde Dehydrogenase 2 ◽  
Logistic Regression Models ◽  
Increased Risk

Abstract Background Alcohol consumption is one of the modifiable risk factors for intracerebral hemorrhage, which accounts for approximately 10–20% of all strokes worldwide. We evaluated the association of stroke with genetic polymorphisms in the alcohol metabolizing genes, alcohol dehydrogenase 1B (ADH1B, rs1229984) and aldehyde dehydrogenase 2 (ALDH2, rs671) genes based on alcohol consumption. Methods Data were available for 19,500 Taiwan Biobank (TWB) participants. We used logistic regression models to test for associations between genetic variants and stroke. Overall, there were 890 individuals with ischemic stroke, 70 with hemorrhagic stroke, and 16,837 control individuals. Participants with ischemic but not hemorrhagic stroke were older than their control individuals (mean  ±  SE, 58.47 ± 8.17 vs. 48.33 ± 10.90 years, p  <  0.0001). ALDH2 rs671 was not associated with either hemorrhagic or ischemic stroke among alcohol drinkers. However, the risk of developing hemorrhagic stroke was significantly higher among ADH1B rs1229984 TC  +  CC individuals who drank alcohol (odds ratio (OR), 4.85; 95% confidence interval (CI) 1.92–12.21). We found that the test for interaction was significant for alcohol exposure and rs1229984 genotypes (p for interaction  =  0.016). Stratification by alcohol exposure and ADH1B rs1229984 genotypes showed that the risk of developing hemorrhagic stroke remained significantly higher among alcohol drinkers with TC  +  CC genotype relative to those with the TT genotype (OR, 4.43, 95% CI 1.19–16.52). Conclusions Our study suggests that the ADH1B rs1229984 TC  +  CC genotype and alcohol exposure of at least 150 ml/week may increase the risk of developing hemorrhagic stroke among Taiwanese adults.

scholarly journals Aldehyde dehydrogenase 2 activity and aldehydic load contribute to neuroinflammation and Alzheimer’s disease related pathology

2019 ◽  
Vol 7 (1) ◽  
Author(s):  
Amit U. Joshi ◽  
Lauren D. Van Wassenhove ◽  
Kelsey R. Logas ◽  
Paras S. Minhas ◽  
Katrin I. Andreasson ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Alcohol Consumption ◽  
Mitochondrial Dysfunction ◽  
Aldehyde Dehydrogenase ◽  
Cortical Neurons ◽  
Aldehyde Dehydrogenase 2 ◽  
East Asians

AbstractAldehyde dehydrogenase 2 deficiency (ALDH2*2) causes facial flushing in response to alcohol consumption in approximately 560 million East Asians. Recent meta-analysis demonstrated the potential link between ALDH2*2 mutation and Alzheimer’s Disease (AD). Other studies have linked chronic alcohol consumption as a risk factor for AD. In the present study, we show that fibroblasts of an AD patient that also has an ALDH2*2 mutation or overexpression of ALDH2*2 in fibroblasts derived from AD patients harboring ApoE ε4 allele exhibited increased aldehydic load, oxidative stress, and increased mitochondrial dysfunction relative to healthy subjects and exposure to ethanol exacerbated these dysfunctions. In an in vivo model, daily exposure of WT mice to ethanol for 11 weeks resulted in mitochondrial dysfunction, oxidative stress and increased aldehyde levels in their brains and these pathologies were greater in ALDH2*2/*2 (homozygous) mice. Following chronic ethanol exposure, the levels of the AD-associated protein, amyloid-β, and neuroinflammation were higher in the brains of the ALDH2*2/*2 mice relative to WT. Cultured primary cortical neurons of ALDH2*2/*2 mice showed increased sensitivity to ethanol and there was a greater activation of their primary astrocytes relative to the responses of neurons or astrocytes from the WT mice. Importantly, an activator of ALDH2 and ALDH2*2, Alda-1, blunted the ethanol-induced increases in Aβ, and the neuroinflammation in vitro and in vivo. These data indicate that impairment in the metabolism of aldehydes, and specifically ethanol-derived acetaldehyde, is a contributor to AD associated pathology and highlights the likely risk of alcohol consumption in the general population and especially in East Asians that carry ALDH2*2 mutation.

Abstract WP497: Investigation of Cognitive Impairment in Ischemic Stroke Patients After Endovascular Treatment in Acute Phase and at 6 Months Follow-Up

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Toru Nakagami ◽  
Satoshi Suda ◽  
Junya Aoki ◽  
Takuya Kanamaru ◽  
Kanako Muraga ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cognitive Impairment ◽  
Cognitive Function ◽  
Endovascular Treatment ◽  
Acute Phase ◽  
Cognitive Assessment ◽  
Internal Carotid ◽  
Stroke Patients ◽  
Number Of Patients

Purpose and Objective: There have been limited reports that focused on cognitive impairment in acute ischemic stroke after endovascular treatment. The aim of this study, therefore, was to investigate cognitive function in patient after endovascular treatment in acute phase and at 6 months follow-up. Method: In this prospective study, from December 2016 to November 2018, the patients who were diagnosed as ischemic stroke with occlusion of the internal carotid artery and of the middle cerebral artery and treated with endovascular treatment were enrolled. Cognitive function was assessed with the Montreal Cognitive Assessment (MoCA-J) test within 5 days of onset and at 6 months follow-up. We defined cognitive impairment as a score of <24 in MoCA-J. Results: 150 patients were enrolled. MoCA-J was feasible in 69 patients (median 76 years; 49 female) (46%), in acute phase (Figure A). 63 patients (91%) had cognitive impairment and no significant differences were found in the naming and the abstraction domains between MoCA-J <24 group and ≧24 group. At 6 months follow-up, 48 patients (median 72 years; 12 female) were assessed with MoCA-J and 35 patients (73%) had cognitive impairment. However, only one patient scored less at 6 months follow-up than in acute phase (Figure B), which resulted in the significant increase in the median MoCA-J score (7 vs. 21, P<0.05) (Figure C) and in all the domains except for the language (P=0.078) (Figure D). Conclusion: In acute phase of ischemic stroke after endovascular treatment, MoCA-J was feasible in about 45%, in which 91% had cognitive impairment. However, at 6 months follow-up, the median MoCA-J score was significantly higher and less number of patients had cognitive impairment. The present results suggest that cognition recovers with time after endovascular treatment in ischemic stroke.

Serum Periostin and Cognitive Impairment in Ischemic Stroke Patients: a Prospective Cohort Study

2021 ◽  
Author(s):  
Guangzong Li ◽  
Jie Li ◽  
Chen Zhu ◽  
Jing Ye ◽  
Bin Wang ◽  
...  
Keyword(s):  
Cohort Study ◽  
Ischemic Stroke ◽  
Cognitive Impairment ◽  
Prospective Cohort Study ◽  
Prospective Cohort ◽  
Enzyme Linked Immunosorbent Assay ◽  
Stroke Severity ◽  
Stroke Patients ◽  
Increased Risk ◽  
Serum Periostin

Abstract Background. Recent evidence suggest elevated periostin is associated with cardiovascular diseases. The aim of this study was to investigate the relationship between serum periostin and post-stroke cognitive impairment (PSCI) at 3 months. Methods. In this prospective cohort study, we enrolled patients with ischemic stroke and hospitalized within 7 days of symptoms onset from January 2019 to January 2020. Serum periostin levels were measured using enzyme-linked immunosorbent assay after admission. Cognitive function assessment was performed at 3-month follow-up visit using the Montreal Cognitive Assessment (MoCA). We defined the PSCI as total MoCA score < 25. Results. A total of 315 ischemic stroke patients were enrolled for the study. PSCI was observed in 173 patients, which accounted for 54.9% (95% confidence interval [CI] 52.1%–57.7%) of the cohort. Serum periostin levels were higher in patients with PSCI than in those without PSCI (median 19.6 vs 14.8 ng/mL; P = 0.001). In logistic regression analysis, the highest quartile of periostin levels were significantly correlated to PSCI (odds ratio [OR], 9.69; 95% CI, 5.06–25.61; P = 0.001), as compared with the lowest quartile. This association remained significant after adjustment for age, gender, educational years, stroke severity, and vascular risk factors. Subgroup analyses further confirmed these results. Furthermore, restricted cubic spline regression demonstrated a linear association between periostin levels and PSCI (P = 0.001 for linearity).Conclusions. This study found that higher serum periostin levels are associated with an increased risk of PSCI at 3 months after ischemic stroke onset.

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