Specific EEG resting state biomarkers in FXS and ASD

IF 4.1 2区医学 Q1 CLINICAL NEUROLOGY

Journal of Neurodevelopmental Disorders Pub Date : 2024-09-09 DOI:10.1186/s11689-024-09570-9

Mélodie Proteau-Lemieux, Inga Sophia Knoth, Saeideh Davoudi, Charles-Olivier Martin, Anne-Marie Bélanger, Valérie Fontaine, Valérie Côté, Kristian Agbogba, Keely Vachon, Kerri Whitlock, Hazel Maridith Barlahan Biag, Angela John Thurman, Cory Rosenfelt, Flora Tassone, Julia Frei, Lucia Capano, Leonard Abbeduto, Sébastien Jacquemont, David Hessl, Randi Jenssen Hagerman, Andrea Schneider, Francois Bolduc, Evdokia Anagnostou, Sarah Lippe

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引用次数: 0

Abstract

Fragile X syndrome (FXS) and autism spectrum disorder (ASD) are neurodevelopmental conditions that often have a substantial impact on daily functioning and quality of life. FXS is the most common cause of inherited intellectual disability (ID) and the most common monogenetic cause of ASD. Previous literature has shown that electrophysiological activity measured by electroencephalogram (EEG) during resting state is perturbated in FXS and ASD. However, whether electrophysiological profiles of participants with FXS and ASD are similar remains unclear. The aim of this study was to compare EEG alterations found in these two clinical populations presenting varying degrees of cognitive and behavioral impairments. Resting state EEG signal complexity, alpha peak frequency (APF) and power spectral density (PSD) were compared between 47 participants with FXS (aged between 5–20), 49 participants with ASD (aged between 6–17), and 52 neurotypical (NT) controls with a similar age distribution using MANCOVAs with age as covariate when appropriate. MANCOVAs controlling for age, when appropriate, and nonverbal intelligence quotient (NVIQ) score were subsequently performed to determine the impact of cognitive functioning on EEG alterations. Our results showed that FXS participants manifested decreased signal complexity and APF compared to ASD participants and NT controls, as well as altered power in the theta, alpha and low gamma frequency bands. ASD participants showed exaggerated beta power compared to FXS participants and NT controls, as well as enhanced low and high gamma power compared to NT controls. However, ASD participants did not manifest altered signal complexity or APF. Furthermore, when controlling for NVIQ, results of decreased complexity in higher scales and lower APF in FXS participants compared to NT controls and ASD participants were not replicated. These findings suggest that signal complexity and APF might reflect cognitive functioning, while altered power in the low gamma frequency band might be associated with neurodevelopmental conditions, particularly FXS and ASD.

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FXS 和 ASD 的特定脑电图静息状态生物标志物

脆性 X 综合征（FXS）和自闭症谱系障碍（ASD）是一种神经发育疾病，通常会对日常功能和生活质量产生重大影响。FXS 是遗传性智力障碍（ID）最常见的病因，也是 ASD 最常见的单基因病因。以往的文献表明，FXS 和 ASD 患者在静息状态下通过脑电图（EEG）测量的电生理活动受到干扰。然而，FXS 和 ASD 患者的电生理特征是否相似仍不清楚。本研究的目的是比较这两种临床人群在不同程度的认知和行为障碍中发现的脑电图改变。研究人员使用 MANCOVA 对 47 名 FXS 患者（年龄在 5-20 岁之间）、49 名 ASD 患者（年龄在 6-17 岁之间）和 52 名年龄分布相似的神经典型（NT）对照者的静息状态脑电信号复杂性、α峰频率（APF）和功率谱密度（PSD）进行了比较。随后进行了控制年龄和非语言智商（NVIQ）得分的 MANCOVA，以确定认知功能对脑电图变化的影响。结果显示，与 ASD 参与者和 NT 对照组相比，FXS 参与者的信号复杂度和 APF 均有所下降，θ、α 和低伽马频段的功率也有所改变。与 FXS 患者和 NT 对照组相比，ASD 患者表现出夸张的 beta 功率，与 NT 对照组相比，则表现出增强的低伽马和高伽马功率。然而，ASD 患者并没有表现出信号复杂性或 APF 的改变。此外，在控制 NVIQ 的情况下，与 NT 对照组和 ASD 参与者相比，FXS 参与者在较高音阶上的复杂性降低和 APF 降低的结果并未得到证实。这些研究结果表明，信号复杂性和APF可能反映了认知功能，而低伽马频段功率的改变可能与神经发育状况有关，尤其是FXS和ASD。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Journal of Neurodevelopmental Disorders 医学-临床神经学

CiteScore

7.60

自引率

4.10%

发文量

审稿时长

>12 weeks

期刊介绍： Journal of Neurodevelopmental Disorders is an open access journal that integrates current, cutting-edge research across a number of disciplines, including neurobiology, genetics, cognitive neuroscience, psychiatry and psychology. The journal’s primary focus is on the pathogenesis of neurodevelopmental disorders including autism, fragile X syndrome, tuberous sclerosis, Turner Syndrome, 22q Deletion Syndrome, Prader-Willi and Angelman Syndrome, Williams syndrome, lysosomal storage diseases, dyslexia, specific language impairment and fetal alcohol syndrome. With the discovery of specific genes underlying neurodevelopmental syndromes, the emergence of powerful tools for studying neural circuitry, and the development of new approaches for exploring molecular mechanisms, interdisciplinary research on the pathogenesis of neurodevelopmental disorders is now increasingly common. Journal of Neurodevelopmental Disorders provides a unique venue for researchers interested in comparing and contrasting mechanisms and characteristics related to the pathogenesis of the full range of neurodevelopmental disorders, sharpening our understanding of the etiology and relevant phenotypes of each condition.