Bui Truong An, Shatto Julie, Cuppens Tania, Droit Arnaud, Bolduc François V
Department of Pediatrics, University of Alberta, Edmonton, AB, Canada.
Centre de Recherche du CHU de Québec-Université Laval et Département de Médecine Moléculaire de l'Université Laval, Laval, QC, Canada.
Front Psychiatry. 2021 Oct 18;12:730987. doi: 10.3389/fpsyt.2021.730987. eCollection 2021.
Fragile X syndrome (FXS) is the most common single-gene cause of intellectual disability and autism spectrum disorder. Individuals with FXS present with a wide range of severity in multiple phenotypes including cognitive delay, behavioral challenges, sleep issues, epilepsy, and anxiety. These symptoms are also shared by many individuals with other neurodevelopmental disorders (NDDs). Since the discovery of the FXS gene, FMR1, FXS has been the focus of intense preclinical investigation and is placed at the forefront of clinical trials in the field of NDDs. So far, most studies have aimed to translate the rescue of specific phenotypes in animal models, for example, learning, or improving general cognitive or behavioral functioning in individuals with FXS. Trial design, selection of outcome measures, and interpretation of results of recent trials have shown limitations in this type of approach. We propose a new paradigm in which all phenotypes involved in individuals with FXS would be considered and, more importantly, the possible interactions between these phenotypes. This approach would be implemented both at the baseline, meaning when entering a trial or when studying a patient population, and also after the intervention when the study subjects have been exposed to the investigational product. This approach would allow us to further understand potential trade-offs underlying the varying effects of the treatment on different individuals in clinical trials, and to connect the results to individual genetic differences. To better understand the interplay between different phenotypes, we emphasize the need for preclinical studies to investigate various interrelated biological and behavioral outcomes when assessing a specific treatment. In this paper, we present how such a conceptual shift in preclinical design could shed new light on clinical trial results. Future clinical studies should take into account the rich neurodiversity of individuals with FXS specifically and NDDs in general, and incorporate the idea of trade-offs in their designs.
脆性X综合征(FXS)是智力障碍和自闭症谱系障碍最常见的单基因病因。患有FXS的个体在多种表型上表现出广泛的严重程度差异,包括认知延迟、行为挑战、睡眠问题、癫痫和焦虑。许多患有其他神经发育障碍(NDDs)的个体也有这些症状。自FXS基因FMR1被发现以来,FXS一直是临床前深入研究的焦点,并处于NDDs领域临床试验的前沿。到目前为止,大多数研究旨在将动物模型中特定表型的挽救转化应用,例如学习能力,或改善FXS患者的一般认知或行为功能。近期试验的试验设计、结局指标的选择以及结果的解释都显示出这种方法存在局限性。我们提出一种新的范式,即考虑FXS患者所涉及的所有表型,更重要的是,考虑这些表型之间可能的相互作用。这种方法将在基线时实施,即在进入试验或研究患者群体时,以及在干预后当研究对象接触了研究产品时。这种方法将使我们能够进一步理解临床试验中治疗对不同个体产生不同影响背后的潜在权衡,并将结果与个体基因差异联系起来。为了更好地理解不同表型之间的相互作用,我们强调临床前研究在评估特定治疗时需要研究各种相互关联的生物学和行为结果。在本文中,我们展示了临床前设计中的这种概念转变如何能够为临床试验结果带来新的启示。未来的临床研究应特别考虑FXS患者以及一般NDDs患者丰富的神经多样性,并在其设计中纳入权衡的理念。