Minimally Verbal ASD: From Basic Mechanisms to Innovative Interventions

最低程度言语自闭症谱系障碍：从基本机制到创新干预措施

• 批准号: 8385988
• 负责人: Helen Tager-Flusberg
• 金额: $ 200.04万
• 依托单位: BOSTON UNIVERSITY (CHARLES RIVER CAMPUS)
• 依托单位国家: 美国
• 财政年份: 2012
• 资助国家: 美国
• 起止时间: 2012-09-04 至 2017-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8385988
• 关键词: Address; Adolescent; Adult; Area; Attention; Auditory; Autistic Disorder; Behavior; Behavioral; Biological; Biological Markers; Boston; Caring; Child; Clinical; Clinical Research; Cognitive; Communication; Communities; Early Diagnosis; Emotional; Failure; Family; Goals; Impairment; Individual; Intervention; Investigation; Knowledge; Language; Lead; Linguistics; Measures; Medical; Medicine; Methods; Minority; Modeling; Molecular; Molecular Target; Nature; Neurobiology; Neurons; Outcome; Outcome Measure; Pathway interactions; Pattern; Perception; Phenotype; Pilot Projects; Population; Production; Proteins; Randomized Clinical Trials; Research; Research Personnel; Research Training; Resolution; Risk; Risk Marker; Safety; School-Age Population; Schools; Series; Societies; Speech; Strategic Planning; Target Populations; Testing; Therapeutic Intervention; Tissue Sample; Toddler; Training and Education; Treatment outcome; Universities; Ursidae Family; autism spectrum disorder; axon growth; base; brain tissue; clinical practice; college; computational neuroscience; data management; design; indexing; infancy; innovation; interest; medical schools; neglect; neuroimaging; novel; relating to nervous system; response; skills; social communication; success; successful intervention; theories; tool; treatment response; white matter

DESCRIPTION: A critical gap identified in the 2011 lACC Strategic Plan is the dearth of knowledge about older children and adults who fail to acquire spoken language. Little is known about these individuals because current assessment tools and practices are not adequate for this population. More significantly, there are no models that explain why about 30% of the ASD population remains minimally verbal and no interventions that specifically and uniquely target this population in promoting spoken language. The goals of our ACE are to address these issues, bringing tools, methods, and approaches have drawn from others areas of speech, auditory, clinical, and computational neurosciences. Our ACE, located at Boston University, brings together researchers from across the university and collaborators from Harvard Medical School, Northeastern University and Albert Einstein College of Medicine. The interconnected projects in the ACE include: a novel intervention to promote spoken language in school-aged children with ASD (Project I); investigation of biological markers of treatment response and outcome (Projects I, II, and III); investigation of mechanisms that might underlie the failure to speak including (a) structural and functional connectivity impairments in key nodes of the speech production network according to the DIVA model (Project 11); (b) abnormalities in the perception, organization and analysis of auditory scenes as indexed in electrophysiological responses and neural oscillatory patterns (Project III); disruptions in excitatory and inhibitory neuronal pathways in key prefrontal cortical areas associated with language using high resolution methods to investigate white matter and axonal growth proteins in tissue samples (Project IV). The projects are united and served by an Administration and Data Management Core (A), a Research Training and Education Core (B) and a Clinical Core (C), which will carry out comprehensive assessments using standard and novel experimental measures to capture the heterogeneous phenotypes of minimally verbal children with ASD, and that will be used to explain variability in treatment response and mechanistic factors identified in the Projects. Together, the research conducted in our ACE will significantly advance our understanding of this neglected end of the autism spectrum, provide innovative approaches to assessment and treatment, pave the way for identifying biological markers predict who will fail to acquire speech, and highlight potential molecular targets for therapeutic interventions.

产品说明：2011年lACC战略计划中确定的一个关键差距是缺乏对未能获得口语的年龄较大的儿童和成人的了解。对这些人知之甚少，因为目前的评估工具和做法不适合这一人群。更重要的是，没有模型可以解释为什么大约30%的ASD人群仍然保持最低限度的语言能力，也没有专门针对这一人群的干预措施来促进口语。我们ACE的目标是解决这些问题，带来的工具，方法和途径已经从语音，听觉，临床和计算神经科学的其他领域得出。我们的ACE位于波士顿大学，汇集了来自整个大学的研究人员和来自哈佛医学院，东北大学和阿尔伯特爱因斯坦医学院的合作者。ACE中相互关联的项目包括：一种促进自闭症学龄儿童口语的新干预措施（项目I）;治疗反应和结局的生物标志物研究（项目一、二和三）;研究可能导致说话失败的机制，包括（a）根据DIVA模型，言语产生网络关键节点的结构和功能连接性损伤（项目11）;（B）听觉场景的感知、组织和分析异常，以电生理反应和神经振荡模式为指标（项目III）;使用高分辨率方法研究与语言相关的关键前额叶皮质区域的兴奋性和抑制性神经元通路的中断组织样本中的白色物质和轴突生长蛋白（项目IV）。这些项目由行政和数据管理核心（A）、研究培训和教育核心（B）以及临床核心（C）联合服务，这些核心将使用标准和新颖的实验措施进行全面评估，以捕获患有ASD的语言能力最低的儿童的异质性表型，并将用于解释项目中确定的治疗反应和机制因素的变异性。总之，在我们的ACE中进行的研究将大大推进我们对自闭症谱系中被忽视的一端的理解，提供创新的评估和治疗方法，为识别生物标记物铺平道路，预测谁将无法获得语言，并突出治疗干预的潜在分子靶点。