HANDEDNESS SUBTYPES--BIOLOGICAL MARKERS IN AUTISM

建议的目标有以下几个方面：（1）确定是否 偏手性分布的变化存在于一个样本中， 自闭症儿童和成人;（2）如果是，以确定其潜在的 结构;（3）确定结构是否是自闭症特有的 还是更普遍地与整体智力迟钝有关 不管自闭症的自闭症和（4），以确定这些是否 表型提供了潜在的不同的神经生物学标志物， 疾病内或疾病间的病因亚组。 受试者将由如下两个自闭症患者样本组成： UCLA样本（n=50），其中包括一个更年轻和更高的功能 （B）Camarillo样本（n=80），其包括老年人和 低功能住院组。 两个功能较低和较高的MR 非自闭症样本将从加州大学洛杉矶分校和卡马里洛州立大学选出 医院作为两个目标样本的对比匹配。 研究设计包括一个为期一周的严格的重测评估， 惯用手使用多个项目正常发育迟缓的SS。 这些措施将用于研究目标1-3， 涉及各种利手表型的鉴定。 一个独特 该项目的特点，包括评估利手，关注 PLH模型（Satz，1972）的扩展，用于处理多利手 表型 这一修订后的模型提供了一个概念和定量的 自闭症患者潜在病因学亚群研究框架 和/或MR受试者。 子类型将首先根据外部行为标准进行验证 以确定它们是否与不同的神经行为结果相关， (e.g.,适应行为，智力，家族利手，营养 四肢的变化）。 如果出现组间差异，作为初步 结果表明，然后每个表型的随机子集将被给予高 分辨率计算机断层扫描，以确定这些表型是否 作为病原亚型的生物学标志物， 婴儿自闭症 该提案旨在解释一些已知的 异质性长期困扰着这种疾病的研究。

The proposed objectives have the following aims: (1) to determine whether a shift in the distribution of handedness exists in an unselected sample of autistic children and adults; (2) if so, to determine its underlying constructs; (3) to determine whether the constructs are specific to autism or whether they relate more generally to overall mental retardation irrespective of autistic symptomatology and (4) to determine whether these phenotypes provide potential neurobiological markers of different etiological subgroups within or between disorders. Subjects will consist of two unselected autistic samples as follows: (a) UCLA Sample (n=50) which comprises a younger and higher functioning outpatient group; (b) Camarillo Sample (n=80) which comprises an older and lower functioning inpatient group. Two lower and higher functioning MR non-autistic samples will be selected from UCLA and Camarillo State Hospital as comparison matches for the two target samples. The research design involves a rigorous one week test-retest assessment of handedness using multiple items normed for developmentally retarded Ss. These measures will be used to investigate Aims 1-3 which essentially involve the identification of various handedness phenotypes. A unique feature of this project, including the assessment of handedness, concerns an extension of the PLH model (Satz, 1972) to deal with multiple handedness phenotypes. This revised model provides a conceptual and quantitative framework for dealing with potential etiological subgroups of autistic and/or MR subjects. The subtypes will first be validated against external behavioral criteria to determine whether they correlate with different neurobehavioral outcomes (e.g., adaptive behavior, intelligence, familial handedness, trophic changes in extremities). If group differences occur, as preliminary results suggest, then a random subset of each phenotype will be given high resolution computerized tomography to determine whether these phenotypes confer any significance as biological markers of etiological subtypes in infantile autism. The proposal seeks to explain some of the known heterogeneity that has long plagued research in this disorder(s).