首页> 美国政府科技报告 >Characterization of the of the Pathological and Biochemical Markers That Correlate to the Clinical Features of Autism. Subproject 2. Contribution of Significant Delay of Neuronal Development and Metabolic Shift of Neurons to Clinical Phenotype of Autism.
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Characterization of the of the Pathological and Biochemical Markers That Correlate to the Clinical Features of Autism. Subproject 2. Contribution of Significant Delay of Neuronal Development and Metabolic Shift of Neurons to Clinical Phenotype of Autism.

机译:与自闭症临床特征相关的病理学和生化标志物的表征。子项目2.神经元显着延迟和神经元代谢转变对自闭症临床表型的贡献。

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The postmortem study of the historically largest cohort including 32 brains of individuals with idiopathic autism, 12 brains of individuals with autism associated with chromosome15 duplication and 28 brains of control subjects, and examination of 36 brain cytoarchitectonic subdivisions was the first attempt to define a global pattern of developmental changes in autism. The study revealed defects of neuronal migration, proliferation and dysplastic changes as a major contributor to seizures. Examination of 2 to 64 year old subjects revealed the first model of brain region-specific modifications of neuron growth trajectories during the lifespan demonstrating desynchronized development of interacting neurons. Neuron soma volume was significantly smaller in all examined regions in 4-8 year old children. Significant increase of neuron size in teenagers and adults to and in some regions above control level without equally significant clinical improvement suggests that delayed growth does not reproduce normal neuronal growth, connectivity and function. Limited alterations in volume of a few structures and number of neurons indicate that alterations of neuronal growth are a major contributor to the clinical autism phenotype.

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