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松果体与自闭症谱系障碍关系的最新观点

Updated View on the Relation of the Pineal Gland to Autism Spectrum Disorders.

作者信息

Shomrat Tal, Nesher Nir

机构信息

Ruppin Academic Center, Faculty of Marine Sciences, Michmoret, Israel.

出版信息

Front Endocrinol (Lausanne). 2019 Feb 5;10:37. doi: 10.3389/fendo.2019.00037. eCollection 2019.

DOI:10.3389/fendo.2019.00037
PMID:30804889
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC6370651/
Abstract

Identification of the biological features of autism is essential for designing an efficient treatment and for prevention of the disorder. Though the subject of extensive research, the neurophysiological features of autism remain unclear. One of the proposed biological causes of autism is malfunction of the pineal gland and deficiency of its principal hormone, melatonin. The main function of melatonin is to link and synchronize the body's homeostasis processes to the circadian and seasonal rhythms, and to regulate the sleep-wake cycle. Therefore, pineal dysfunction has been implicated based on the common observation of low melatonin levels and sleep disorders associated with autism. In this perspective, we highlight several recent findings that support the hypothesis of pineal gland/melatonin involvement in autism. Another common symptom of autism is abnormal neuroplasticity, such as cortical overgrowth and dendritic spine dysgenesis. Here, we synthesize recent information and speculate on the possibility that this abnormal neuroplasticity is caused by hyperactivity of endogenous N,N-dimethyltryptamine (DMT). The pineal gland was proposed as the source of DMT in the brain and therefore, our assumption is that besides melatonin deficiency, pineal dysfunction might also play a part in the development of autism through abnormal metabolism of DMT. We hope that this manuscript will encourage future research of the DMT hypothesis and reexamination of several observations that were previously attributed to other factors, to see if they could be related to pineal gland/melatonin malfunction. Such research could contribute to the development of autism treatment by exogenous melatonin and monitored light exposure.

摘要

识别自闭症的生物学特征对于设计有效的治疗方法和预防该疾病至关重要。尽管自闭症是广泛研究的主题,但其神经生理学特征仍不清楚。自闭症的一种可能生物学原因是松果体功能失调及其主要激素褪黑素缺乏。褪黑素的主要功能是将身体的内稳态过程与昼夜节律和季节节律联系起来并使其同步,以及调节睡眠-觉醒周期。因此,基于与自闭症相关的褪黑素水平低和睡眠障碍的常见观察结果,松果体功能障碍被牵连其中。从这个角度出发,我们强调了一些最近的发现,这些发现支持松果体/褪黑素与自闭症有关的假说。自闭症的另一个常见症状是异常的神经可塑性,如皮质过度生长和树突棘发育异常。在此,我们综合了最近的信息,并推测这种异常神经可塑性是由内源性N,N-二甲基色胺(DMT)活性过高引起的可能性。松果体被认为是大脑中DMT的来源,因此,我们的假设是,除了褪黑素缺乏外,松果体功能障碍可能还通过DMT的异常代谢在自闭症的发展中起作用。我们希望这篇手稿将鼓励未来对DMT假说的研究,并重新审视一些以前归因于其他因素的观察结果,看看它们是否可能与松果体/褪黑素功能障碍有关。这样的研究可能有助于通过外源性褪黑素和监测光照来开发自闭症治疗方法。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efb7/6370651/c6079390c2a9/fendo-10-00037-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efb7/6370651/c6079390c2a9/fendo-10-00037-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/efb7/6370651/c6079390c2a9/fendo-10-00037-g0001.jpg

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Modulating autism spectrum disorder pathophysiology using a trace amine-focused approach: targeting the gut.
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