Abstract：
BACKGROUND: Compared with conventional unimodal analysis, understanding how brain function and structure relate to one another opens a new biologically relevant assessment of neural mechanisms. However, how function-structure dependencies (FSDs) evolve throughout typical and abnormal neurodevelopment remains elusive. The 22q11.2 deletion syndrome (22q11.2DS) offers an important opportunity to study the development of FSDs and their specific association with the pathophysiology of psychosis.
METHODS: Previously, we used graph signal processing to combine brain activity and structural connectivity measures in adults, quantifying FSD. Here, we combined FSD with longitudinal multivariate partial least squares correlation to evaluate FSD alterations across groups and among patients with and without mild to moderate positive psychotic symptoms. We assessed 391 longitudinally repeated resting-state functional and diffusion-weighted magnetic resonance images from 194 healthy control participants and 197 deletion carriers (ages 7-34 years, data collected over a span of 12 years).
RESULTS: Compared with control participants, patients with 22q11.2DS showed a persistent developmental offset from childhood, with regions of hyper- and hypocoupling across the brain. Additionally, a second deviating developmental pattern showed an exacerbation during adolescence, presenting hypocoupling in the frontal and cingulate cortices and hypercoupling in temporal regions for patients with 22q11.2DS. Interestingly, the observed aggravation during adolescence was strongly driven by the group with positive psychotic symptoms.
CONCLUSIONS: These results confirm a central role of altered FSD maturation in the emergence of psychotic symptoms in 22q11.2DS during adolescence. The FSD deviations precede the onset of psychotic episodes and thus offer a potential early indication for behavioral interventions in individuals at risk.
METHODS: Previously, we used graph signal processing to combine brain activity and structural connectivity measures in adults, quantifying FSD. Here, we combined FSD with longitudinal multivariate partial least squares correlation to evaluate FSD alterations across groups and among patients with and without mild to moderate positive psychotic symptoms. We assessed 391 longitudinally repeated resting-state functional and diffusion-weighted magnetic resonance images from 194 healthy control participants and 197 deletion carriers (ages 7-34 years, data collected over a span of 12 years).
RESULTS: Compared with control participants, patients with 22q11.2DS showed a persistent developmental offset from childhood, with regions of hyper- and hypocoupling across the brain. Additionally, a second deviating developmental pattern showed an exacerbation during adolescence, presenting hypocoupling in the frontal and cingulate cortices and hypercoupling in temporal regions for patients with 22q11.2DS. Interestingly, the observed aggravation during adolescence was strongly driven by the group with positive psychotic symptoms.
CONCLUSIONS: These results confirm a central role of altered FSD maturation in the emergence of psychotic symptoms in 22q11.2DS during adolescence. The FSD deviations precede the onset of psychotic episodes and thus offer a potential early indication for behavioral interventions in individuals at risk.
摘要：
背景：了解大脑功能和结构如何相互关联，与传统的单峰分析相比，开启了一种新的神经机制的生物学相关评估。然而,在整个典型和异常的神经发育过程中，功能结构依赖性如何演变仍然难以捉摸。22q11.2缺失综合征（22q11.2DS）为研究功能结构依赖性的发展及其与精神病病理生理学的特定关联提供了重要机会。
方法：以前，我们使用图形信号处理来结合成人的大脑活动和结构连通性测量，量化功能-结构依赖性(FSD)。这里,我们将FSD与纵向多变量偏最小二乘相关(PLS-C)相结合,以评估各组间以及有或无轻度至中度精神病性症状(PPS)的患者中的FSD改变.我们评估了194名健康对照和197名缺失携带者的391个纵向重复静息态功能和扩散加权磁共振成像（年龄7-34岁，数据收集时间为12年）结果：相对于对照，22q11.2DS患者表现出持续的儿童期发育偏移，大脑中的高耦合和低耦合区域。此外,第二个偏离的发育模式显示青春期恶化，22q11.2D患者的额叶和扣带皮质呈现低耦合，颞区呈现高耦合。有趣的是,在青春期观察到的加重是由PPS+组强烈驱动的.
结论：这些结果证实了FSD成熟改变在青春期22q11.2DS精神病症状出现中的重要作用。FSD偏差先于精神病发作发作，因此为处于危险中的个体的行为干预提供了潜在的早期指示。
方法：以前，我们使用图形信号处理来结合成人的大脑活动和结构连通性测量，量化功能-结构依赖性(FSD)。这里,我们将FSD与纵向多变量偏最小二乘相关(PLS-C)相结合,以评估各组间以及有或无轻度至中度精神病性症状(PPS)的患者中的FSD改变.我们评估了194名健康对照和197名缺失携带者的391个纵向重复静息态功能和扩散加权磁共振成像（年龄7-34岁，数据收集时间为12年）结果：相对于对照，22q11.2DS患者表现出持续的儿童期发育偏移，大脑中的高耦合和低耦合区域。此外,第二个偏离的发育模式显示青春期恶化，22q11.2D患者的额叶和扣带皮质呈现低耦合，颞区呈现高耦合。有趣的是,在青春期观察到的加重是由PPS+组强烈驱动的.
结论：这些结果证实了FSD成熟改变在青春期22q11.2DS精神病症状出现中的重要作用。FSD偏差先于精神病发作发作，因此为处于危险中的个体的行为干预提供了潜在的早期指示。
