基于促进脑酶的自闭症修饰疗法:一个介绍性病例报告

IF 0.7 Q4 BIOCHEMISTRY & MOLECULAR BIOLOGY
D. Béroule
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引用次数: 2

摘要

一项关于自闭症的跨学科研究表明,突触血清素(一种与大脑发育有关的分子)的降解相对较差。由此产生的单胺类神经递质代谢失衡被认为会阻碍睡眠阶段的记忆编码,从而导致与自闭症症状相关的异常神经结构的形成。从这种理论方法中可以衍生出一种药物,其目的是调节神经调节,从而使正常的神经网络开始在受损的神经网络上生长。丙戊酸抗惊厥药在这里的作用是促进一种相关的脑酶,即单胺氧化酶a (MAOA)。虽然个案研究通常集中在轻度到中度自闭症中不到三个月的症状子集,但在一个患有严重自闭症的11岁男孩身上,每一种自闭症症状的演变都被见证了一年。9个月后,随着睡眠的快速改善,视觉探索能力的增强,核心症状出现了明显的积极变化,但仍然受到多动发作的阻碍。在不干扰丙戊酸的情况下,服用哌醋甲酯精神兴奋剂可以增加注意力的持续时间。这种maoa诱导剂和精神兴奋剂的组合最终有利于社会条件的逐渐获得,但没有完全消除10年自闭症形成的不良习惯。由于仅限于改善疾病的作用,这种双重治疗依赖于伴随的教育援助,特别是从其探索性监测中了解到。其他见解侧重于特定的生物标志物以及相关基因启动子的功能多态性,旨在指导未来的临床试验。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Autism-modifying therapy based on the promotion of a brain enzyme: An introductory case-report
An interdisciplinary study of autism led to implicate the relatively poor degradation of synaptic serotonin , a molecule involved in brain development. Consequent metabolic imbalance of monoamine neurotransmitters is assumed to impede memory encoding across sleep stages, hence the building of aberrant neural structures linked with autistic symptoms. A medication can be derived from this theoretical approach, with the aim of regulating neuromodulation whereby proper neural networks may start growing over impaired ones. The Valproate anticonvulsant has been prescribed here for its contribution to the promotion of a relevant brain enzyme known as Monoamine oxidase A (MAOA). Whereas case-studies usually focus on a subset of symptoms for less than three months in mild to moderate autism, the evolution of every autistic symptom has been witnessed across one year in an 11-year boy with severe autism. Rapid improvement of sleep, followed by the rising of visual exploration, preceded positive shifts of the core symptoms noticeable nine months later, however still impeded by bursts of hyperactivity. The adjunctive medication of Methylphenidate psychostimulant permitted afterwards to increase the attention span without interfering with Valproate. Such combination of MAOA-inducer and psychostimulant eventually favored the gradual acquisition of social conditioning, without fully erasing poor habits issued from ten years of autism. Because restricted to a disease-modifying action, this dual therapy relies on accompanying educational assistance, as notably learnt from its exploratory monitoring. Other insights focus on specific biomarkers as well as functional polymorphisms of relevant genes promoters, with the aim of guiding future clinical trials.
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来源期刊
AIMS Molecular Science
AIMS Molecular Science BIOCHEMISTRY & MOLECULAR BIOLOGY-
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