<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-09-19T00:54:37Z</responseDate><request verb="GetRecord" identifier="oai:dspace.mit.edu:1721.1/73775" metadataPrefix="dim">https://dspace.mit.edu/server/oai/request</request><GetRecord><record><header><identifier>oai:dspace.mit.edu:1721.1/73775</identifier><datestamp>2022-01-13T07:54:17Z</datestamp><setSpec>com_1721.1_7582</setSpec><setSpec>com_1721.1_7581</setSpec><setSpec>col_1721.1_131022</setSpec></header><metadata><dim:dim xmlns:dim="http://www.dspace.org/xmlns/dspace/dim" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.dspace.org/xmlns/dspace/dim http://www.dspace.org/schema/dim.xsd">
   <dim:field mdschema="dc" element="contributor" qualifier="advisor" lang="en_US">Li-Huei Tsai.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="author" lang="en_US">Soda, Takahiro</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="other" lang="en_US">Massachusetts Institute of Technology. Dept. of Brain and Cognitive Sciences.</dim:field>
   <dim:field mdschema="dc" element="contributor" qualifier="department">Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="accessioned">2012-10-10T15:44:10Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="available">2012-10-10T15:44:10Z</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="copyright" lang="en_US">2012</dim:field>
   <dim:field mdschema="dc" element="date" qualifier="issued" lang="en_US">2012</dim:field>
   <dim:field mdschema="dc" element="identifier" qualifier="uri">http://hdl.handle.net/1721.1/73775</dim:field>
   <dim:field mdschema="dc" element="identifier" qualifier="oclc" lang="en_US">810144278</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Brain and Cognitive Sciences, 2012.</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Cataloged from PDF version of thesis.</dim:field>
   <dim:field mdschema="dc" element="description" lang="en_US">Includes bibliographical references.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="abstract" lang="en_US">According to the World Health Organization, neuropsychiatric diseases account for approximately one third of years lost to disability. Yet, despite this huge disease burden, there is a lack of new treatments under development: approved treatments all essentially target the same target(s), if the target itself is known. There is now considerable evidence for a common set of heritable risk for psychiatric disorders including schizophrenia, bipolar disorder, as well as autism. Many of these risk alleles affect genes implicated in neuronal development with known roles at an early stage; these genes would have an effect on the individual before the onset of overt symptoms or diagnosis. Furthermore, many of the genes identified are known to participate in established pathways that are relevant for neuronal development and function. It is important then to address the causality between these signaling pathways that are important for neurodevelopment, and the risk of developing neuropsychiatric disorder. The work presented in this thesis represents two projects that aim to work toward this goal. The first project pertains to the mechanisms of transcriptional repression by DISC1 on ATF4-mediated gene transcription. The second project presents some initial steps towards uncovering the role of BCL9 in neuronal development.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="statementofresponsibility" lang="en_US">by Takahiro Soda.</dim:field>
   <dim:field mdschema="dc" element="description" qualifier="degree" lang="en_US">Ph.D.</dim:field>
   <dim:field mdschema="dc" element="format" qualifier="extent" lang="en_US">131 p.</dim:field>
   <dim:field mdschema="dc" element="language" qualifier="iso" lang="en_US">eng</dim:field>
   <dim:field mdschema="dc" element="publisher" lang="en_US">Massachusetts Institute of Technology</dim:field>
   <dim:field mdschema="dc" element="rights" lang="en_US">M.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.</dim:field>
   <dim:field mdschema="dc" element="rights" qualifier="uri" lang="en_US">http://dspace.mit.edu/handle/1721.1/7582</dim:field>
   <dim:field mdschema="dc" element="subject" lang="en_US">Brain and Cognitive Sciences.</dim:field>
   <dim:field mdschema="dc" element="title" lang="en_US">Converging biochemical pathways in psychiatric disorders</dim:field>
   <dim:field mdschema="dc" element="title" qualifier="alternative" lang="en_US">biological role in genes that confer risk to psychiatric disorders</dim:field>
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   	&lt;Title>Converging biochemical pathways in psychiatric disorders&lt;/Title>
   	&lt;Subtitle>biological role in genes that confer risk to psychiatric disorders&lt;/Subtitle>
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   	&lt;PublicationDate>2012&lt;/PublicationDate>
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            &lt;DisplayName>Massachusetts Institute of Technology&lt;/DisplayName>
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    &lt;Keyword>Brain and Cognitive Sciences.&lt;/Keyword>
   	&lt;Abstract>According to the World Health Organization, neuropsychiatric diseases account for approximately one third of years lost to disability. Yet, despite this huge disease burden, there is a lack of new treatments under development: approved treatments all essentially target the same target(s), if the target itself is known. There is now considerable evidence for a common set of heritable risk for psychiatric disorders including schizophrenia, bipolar disorder, as well as autism. Many of these risk alleles affect genes implicated in neuronal development with known roles at an early stage; these genes would have an effect on the individual before the onset of overt symptoms or diagnosis. Furthermore, many of the genes identified are known to participate in established pathways that are relevant for neuronal development and function. It is important then to address the causality between these signaling pathways that are important for neurodevelopment, and the risk of developing neuropsychiatric disorder. The work presented in this thesis represents two projects that aim to work toward this goal. The first project pertains to the mechanisms of transcriptional repression by DISC1 on ATF4-mediated gene transcription. The second project presents some initial steps towards uncovering the role of BCL9 in neuronal development.&lt;/Abstract>
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