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dc.contributor.advisorKenneth N. Wexler.en_US
dc.contributor.authorModyanova, Nadezhda Nen_US
dc.contributor.otherMassachusetts Institute of Technology. Dept. of Brain and Cognitive Sciences.en_US
dc.date.accessioned2010-08-26T15:22:36Z
dc.date.available2010-08-26T15:22:36Z
dc.date.copyright2009en_US
dc.date.issued2009en_US
dc.identifier.urihttp://hdl.handle.net/1721.1/57547
dc.descriptionThesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2009.en_US
dc.descriptionThis electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.en_US
dc.descriptionCataloged from student submitted PDF version of thesis.en_US
dc.descriptionIncludes bibliographical references.en_US
dc.description.abstractThe elucidation of the biological bases of a complex trait like human language proceeds from identification of precise behavioral phenotypes to investigation of the underlying genes. The human behavioral parts of this dissertation focus on understanding the reasons for children's overuse of definite article 'the', to refer to one of several objects in a context set, as opposed to the unique established referent. Competing theories argue the deficit is either in children's semantic computational knowledge (of uniqueness/maximality), or in their pragmatic/social awareness/theory-of-mind development. Experiments in this dissertation focused on children's comprehension and interpretation of the indefinite and definite determiners, as well as 'that', anaphors 'another' and 'same', and free relative clauses. The results in this thesis suggest that in typically developing (TD) children the late acquisition of determiner 'the' is due to the late maturation of the semantic principle of maximality. Children with autism spectrum disorders (ASD) and with Williams syndrome (WS) either manifested an adult-like competence, an absence of manifestation of knowledge, or a pattern found in TD younger children (where 'that' is understood better than 'the' as referring to the salient unique referent) -- indicating delay of development of the language faculty, but no deviance. This suggests that the observed deficits in ASD and WS pattern with those in TD, and hence are also semantic in nature. The mouse neurogenetic part of this dissertation investigates whether the GTF2I family of genes, causal to WS behavioral phenotype, also contributes to WS cortical development.en_US
dc.description.abstract(cont.) By overexpression of Gtf2i and Gtf2ird1 in the mouse neocortex via in utero electroporation, their effects on laminar patterning and cell morphogenesis during brain development are characterized. The present results suggest that these genes can synergistically contribute to the abnormal neocortical development in WS, and thereby could contribute to language deficits in WS. Beyond posing an explanatory challenge to linguistic theories, the research comparing typical and atypical development sheds light on the mechanisms of language development and impairment, and provides endophenotypic descriptions of ASD and WS, which are crucial for elucidating not only genetics of neurodevelopmental disorders, but also the genetic basis of the human language faculty.en_US
dc.description.statementofresponsibilityby Nadezhda N. Modyanova.en_US
dc.format.extent161 p.en_US
dc.language.isoengen_US
dc.publisherMassachusetts Institute of Technologyen_US
dc.rightsM.I.T. theses are protected by copyright. They may be viewed from this source for any purpose, but reproduction or distribution in any format is prohibited without written permission. See provided URL for inquiries about permission.en_US
dc.rights.urihttp://dspace.mit.edu/handle/1721.1/7582en_US
dc.subjectBrain and Cognitive Sciences.en_US
dc.titleSemantic and pragmatic language development in typical acquisition, autism spectrum disorders, and Williams syndrome with reference to developmental neurogenetics of the latteren_US
dc.typeThesisen_US
dc.description.degreePh.D.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Dept. of Brain and Cognitive Sciences.en_US
dc.identifier.oclc639300313en_US


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