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自闭症的神经发育:关键时期、压力与营养

Neurodevelopment of Autism: Critical Periods, Stress and Nutrition.

作者信息

Ayoub George

机构信息

Psychology, Santa Barbara City College, Santa Barbara, CA 93109, USA.

出版信息

Cells. 2024 Nov 28;13(23):1968. doi: 10.3390/cells13231968.

DOI:10.3390/cells13231968
PMID:39682717
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11640478/
Abstract

Autism spectrum disorder (ASD) is a neurodevelopmental disability that presents significant challenges in communication and behavior. ASD prevalence exceeds 2% among eight-year-old children and is at similar levels globally. We propose that critical periods during fetal development and early postnatal years establish the conditions for either neurotypical development or the emergence of autism through mechanisms that influence immune function or delay neuronal development. One critical period is characterized by the requirement for folate, a crucial methyl donor needed for DNA regulation. Insufficient folate availability has been linked to the risk of developing ASD. Another critical period may be affected by oxidative stress or inflammation of the fetal brain, potentially due to inadequate microglial immunity, which can lead to CNS inflammatory changes that disrupt typical neurodevelopment. We suggest that early supplementation with reduced folate and taurine during both the fetal and postnatal stages may be effective in mitigating the severity of ASD symptoms by promoting neurotypical development through these critical neurodevelopmental periods.

摘要

自闭症谱系障碍(ASD)是一种神经发育障碍,在沟通和行为方面带来重大挑战。ASD在八岁儿童中的患病率超过2%,且在全球范围内处于相似水平。我们提出,胎儿发育和出生后早期的关键时期通过影响免疫功能或延迟神经元发育的机制,为神经典型发育或自闭症的出现奠定了条件。一个关键时期的特点是对叶酸有需求,叶酸是DNA调节所需的关键甲基供体。叶酸供应不足与患ASD的风险有关。另一个关键时期可能受胎儿大脑氧化应激或炎症的影响,这可能是由于小胶质细胞免疫不足所致,可导致中枢神经系统炎症变化,扰乱典型的神经发育。我们建议,在胎儿期和出生后阶段早期补充还原型叶酸和牛磺酸,可能通过在这些关键神经发育时期促进神经典型发育,有效减轻ASD症状的严重程度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba41/11640478/f03ab6b970a8/cells-13-01968-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba41/11640478/f03ab6b970a8/cells-13-01968-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ba41/11640478/f03ab6b970a8/cells-13-01968-g001.jpg

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本文引用的文献

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Adv Nutr. 2024 Sep;15(9):100279. doi: 10.1016/j.advnut.2024.100279. Epub 2024 Jul 24.
2
Variations in folate prescriptions for patients with the MTHFR genetic polymorphisms: A case series study.MTHFR基因多态性患者叶酸处方的差异:一项病例系列研究。
Explor Res Clin Soc Pharm. 2023 May 8;10:100277. doi: 10.1016/j.rcsop.2023.100277. eCollection 2023 Jun.
3
Altered behavior, brain structure, and neurometabolites in a rat model of autism-specific maternal autoantibody exposure.
自闭症特异性母体自身抗体暴露的大鼠模型中的行为改变、大脑结构和神经代谢产物。
Mol Psychiatry. 2023 May;28(5):2136-2147. doi: 10.1038/s41380-023-02020-3. Epub 2023 Mar 27.
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Comorbidities in autism spectrum disorder and their etiologies.自闭症谱系障碍中的共病及其病因。
Transl Psychiatry. 2023 Feb 25;13(1):71. doi: 10.1038/s41398-023-02374-w.
5
Critical periods and Autism Spectrum Disorders, a role for sleep.关键期与自闭症谱系障碍:睡眠的作用
Neurobiol Sleep Circadian Rhythms. 2022 Dec 20;14:100088. doi: 10.1016/j.nbscr.2022.100088. eCollection 2023 May.
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Maternal autoantibody profiles as biomarkers for ASD and ASD with co-occurring intellectual disability.母体自身抗体谱作为 ASD 及伴发智力障碍 ASD 的生物标志物。
Mol Psychiatry. 2022 Sep;27(9):3760-3767. doi: 10.1038/s41380-022-01633-4. Epub 2022 May 26.
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