Delhey Leanna M, Tippett Marie, Rose Shannon, Bennuri Sirish C, Slattery John C, Melnyk Stepan, James S Jill, Frye Richard E
Arkansas Children's Research Institute, Little Rock, AR, United States.
Department of Epidemiology, Fay W. Boozman College of Public Health, University of Arkansas for Medical Sciences, Little Rock, AR, United States.
Front Neurosci. 2018 Feb 12;12:19. doi: 10.3389/fnins.2018.00019. eCollection 2018.
Autism spectrum disorder (ASD) affects about 1 in 45 individuals in the United States, yet effective treatments are yet to be defined. There is growing evidence that ASD is associated with abnormalities in several metabolic pathways, including the inter-connected folate, methylation and glutathione pathways. Several treatments that can therapeutically target these pathways have been tested in preliminary clinical trials. The combination of methylcobalamin (mB12) with low-dose folinic acid (LDFA) and sapropterin, a synthetic form of tetrahydrobiopterin (BH4) have been studied in open-label trials while high-dose folinic acid has been studied in a double-blind placebo controlled trial. All of these treatments have the potential to positively affect folate, methylation and glutathione pathways. Although the effect of mB12/LDFA and BH4 on methylation and glutathione metabolism have been examined in the open-label studies, these changes have not been compared to controls who received a placebo in order to account for the natural variation in the changes in these pathways. Furthermore, the recent study using high-dose folinic acid (HDFA) did not analyze the change in metabolism resulting from the treatment. Thus, we compared changes in methylation and glutathione metabolism and biomarkers of chronic oxidative stress as a result of these three treatments to individuals receiving placebo. In general, mB12/LDFA treatment had a significant effect on glutathione and cysteine metabolism with a medium effect size while BH4 had a significant effect on methylation and markers of chronic oxidative stress with a large effect size. HDFA treatment did not significantly influence biomarkers of methylation, glutathione or chronic oxidative stress. One caveat was that participants in the mB12/LDFA and BH4 studies had significantly worse markers of glutathione metabolism and chronic oxidative stress at baseline, respectively. Thus, the participants selected in these two clinical trials may have been those with the most severe metabolic abnormalities and most expected to respond to these treatments. Overall this study supports the notion that metabolic abnormalities in individuals with ASD may be amenable to targeted treatments and provide some insight into the mechanism of action of these treatments.
在美国,自闭症谱系障碍(ASD)影响着约每45人中的1人,但尚未确定有效的治疗方法。越来越多的证据表明,ASD与多种代谢途径的异常有关,包括相互关联的叶酸、甲基化和谷胱甘肽途径。几种可以针对这些途径进行治疗的方法已在初步临床试验中进行了测试。甲钴胺(mB12)与低剂量亚叶酸(LDFA)以及四氢生物蝶呤(BH4)的合成形式沙丙蝶呤的组合已在开放标签试验中进行了研究,而高剂量亚叶酸已在双盲安慰剂对照试验中进行了研究。所有这些治疗方法都有可能对叶酸、甲基化和谷胱甘肽途径产生积极影响。尽管在开放标签研究中已经研究了mB12/LDFA和BH4对甲基化和谷胱甘肽代谢的影响,但这些变化尚未与接受安慰剂的对照组进行比较,以便考虑这些途径变化中的自然变异。此外,最近使用高剂量亚叶酸(HDFA)的研究没有分析治疗引起的代谢变化。因此,我们将这三种治疗方法导致的甲基化和谷胱甘肽代谢变化以及慢性氧化应激生物标志物与接受安慰剂的个体进行了比较。总体而言,mB12/LDFA治疗对谷胱甘肽和半胱氨酸代谢有显著影响,效应大小为中等,而BH4对甲基化和慢性氧化应激标志物有显著影响,效应大小为大。HDFA治疗对甲基化、谷胱甘肽或慢性氧化应激的生物标志物没有显著影响。一个需要注意的是,mB12/LDFA和BH4研究中的参与者在基线时谷胱甘肽代谢和慢性氧化应激的标志物分别明显更差。因此,这两项临床试验中选择的参与者可能是那些代谢异常最严重且最有望对这些治疗产生反应的人。总体而言,这项研究支持了ASD个体的代谢异常可能适合靶向治疗的观点,并为这些治疗的作用机制提供了一些见解。