Low maternal melatonin level increases autism spectrum disorder risk in children
Low maternal melatonin level increases autism spectrum disorder risk in children
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DOI：
10.1016/j.ridd.2018.02.017
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发表时间：
2018-11-01
影响因子：
3.1
通讯作者：
Curfs, Leopold
中科院分区：
文献类型：
--
作者：
Braam, Wiebe;Ehrhart, Friederike;Curfs, Leopold
背景资料：自闭症谱系障碍（ASD）被认为是由从头遗传变异和共同变异以及环境因素的组合引起的。它经常与智力残疾（ID）共存。在ASD患者中发现了近800种潜在的致病基因变异。然而，其中没有一个是负责超过1%的ASD病例。低褪黑激素水平是ASD患者的常见发现。褪黑激素水平与自闭症障碍的严重程度呈负相关，它对正常的神经发育很重要，并且在保护DNA免受氧化损伤方面非常有效。褪黑激素缺乏可能是一个主要因素，以及一个共同的遗传变异，增加了对ASD的环境危险因素的易感性。ASD在出生时就已经存在。由于胎儿不产生褪黑激素，低产妇褪黑激素水平可能involved.Methods：我们测量了6-sulfatoxymelatonin尿液中的60名母亲的儿童与ASD和controls.Results：6-sulfatoxymelatonin水平显着低于母亲与ASD儿童比在controls.Conclusions：低父母褪黑激素水平可能是一个贡献者ASD和可能的ID病因。我们的发现需要在更大的范围内进行复制。如果我们的假设是正确的，这可能会导致政策，以检测未来的父母谁是风险和治疗策略，以ASD和智力残疾的风险。
Background: It is assumed that autism spectrum disorder (ASD) is caused by a combination of de novo inherited variation and common variation as well as environmental factors. It often cooccurs with intellectual disability (ID). Almost eight hundred potential causative genetic variations have been found in ASD patients. However, not one of them is responsible for more than 1% of ASD cases. Low melatonin levels are a frequent finding in ASD patients. Melatonin levels are negatively correlated with severity of autistic impairments, it is important for normal neurodevelopment and is highly effective in protecting DNA from oxidative damage. Melatonin deficiency could be a major factor, and well a common heritable variation, that increases the susceptibility to environmental risk factors for ASD. ASD is already present at birth. As the fetus does not produce melatonin, low maternal melatonin levels may be involved.Methods: We measured 6-sulfatoxymelatonin in urine of 60 mothers of a child with ASD and controls.Results: 6-sulfatoxymelatonin levels were significantly lower in mothers with an ASD child than in controls (p = 0.012).Conclusions: Low parental melatonin levels could be one of the contributors to ASD and possibly ID etiology. Our findings need to be duplicated on a larger scale. If our hypothesis is correct, this could lead to policies to detect future parents who are at risk and to treatment strategies to ASD and intellectual disability risk.