Abstract
Recent studies have demonstrated the protective effect of mitochondrial aldehyde dehydrogenase 2 (ALDH2) in cardiovascular diseases. Increased levels of the potential ALDH2 substrate 4-hydroxynonenal (4-HNE) are involved in myocardial/cerebral ischemia accompanied by a high level of oxidative stress. In this investigation, we first performed a case-control study to explore the potential association of ALDH2 rs671 polymorphism and post-stroke epilepsy (PSE). Then, we performed an in vitro study to determine whether the overexpression of ALDH2 could decrease the level of oxidative stress and the apoptosis ratio induced by 4-HNE. There was a significant difference in the distribution of the allele and genotype frequencies of the rs671 polymorphism between PSE patients and ischemic stroke (IS) patients. Individuals with the rs671 A allele showed significantly higher levels of plasma 4-HNE. The overexpression of ALDH2 partially blocked the increased levels of malondialdehyde (MDA), reactive oxygen species (ROS) and apoptosis ratio induced by 4-HNE and also partially restored the ALDH2 activity in PC12 cells; these effects were reversed in the presence of εV1-2. Our results suggest that the ALDH2 rs671 polymorphism is associated with PSE susceptibility and affects the 4-HNE levels. Targeting ALDH2 might be a useful strategy for the treatment or prevention of PSE.
Highlights
Epilepsy is the second most common disease of the nervous system only after cerebrovascular disease [1]
When the groups were stratified according to history of alcohol consumption, a more significant difference in the frequency of the rs671 A allele was found in the subjects with a negative history of alcohol consumption (37.5% vs 24.3%, P = 0.00010, OR = 2.37, 95%CI = 1.54–3.65)
Using a case-control study, we demonstrated that the functional single nucleotide polymorphism (SNP) rs671 of aldehyde dehydrogenase 2 (ALDH2) is associated with post-stroke epilepsy
Summary
Epilepsy is the second most common disease of the nervous system only after cerebrovascular disease [1]. Epilepsy is caused by a variety of pathogenic factors and has been shown to be a chronic, recurrent, transient syndrome resulting from brain dysfunction. This condition is characterized by abnormal discharge in brain neurons, and the frequent attacks cause progressive damage to brain neurons. Post-stroke epilepsy has a negative effect on stroke prognosis and the quality of life. A Canadian research group reported that post-stroke epilepsy was associated with an increased utilization of resources, an increased length of hospital stay and a decrease in both the 30-day and 1year survival rates [4]. The identification of a new method for predicting the occurrence of post-stroke epilepsy may result in the development of new strategies for the prevention and treatment of post-stroke epilepsy
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