<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/">
<rdf:Description rdf:about="https://riquim.fq.edu.uy/items/show/6999">
    <dcterms:title><![CDATA[<strong>Untargeted metabolomics of 3xTg-AD neurotoxic astrocytes</strong>]]></dcterms:title>
    <dcterms:subject><![CDATA[SISTEMA NERVIOSO]]></dcterms:subject>
    <dcterms:subject><![CDATA[FLAVONOIDES]]></dcterms:subject>
    <dcterms:subject><![CDATA[FENOTIPO]]></dcterms:subject>
    <dcterms:subject><![CDATA[ENFERMEDADES NEUROMUSCULARES]]></dcterms:subject>
    <dcterms:subject><![CDATA[ASTROCITOS]]></dcterms:subject>
    <dcterms:subject><![CDATA[NEURODEGENERACION]]></dcterms:subject>
    <dcterms:subject><![CDATA[TRANSCRIPTOMICA]]></dcterms:subject>
    <dcterms:subject><![CDATA[METABOLOMICA]]></dcterms:subject>
    <dcterms:subject><![CDATA[ENFERMEDAD DE ALZHEIMER]]></dcterms:subject>
    <dcterms:subject><![CDATA[RATONES 3x-Tg-AD]]></dcterms:subject>
    <dcterms:subject><![CDATA[DEMENCIA]]></dcterms:subject>
    <dcterms:subject><![CDATA[BIBLIOGRAFIA NACIONAL QUIMICA]]></dcterms:subject>
    <dcterms:subject><![CDATA[2025]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Alzheimer’s disease (AD) is the most common form of dementia, affecting approximately 47 M people worldwide. Histological features and genetic risk factors, among other evidence, supported the amyloid hypothesis of the disease. This neuronocentric paradigm is currently undergoing a shift, considering evidence of the role of other cell types, such as microglia and astrocytes, in disease progression. Previously, we described a particular astrocyte subtype obtained from the 3xTg-AD murine model that displays neurotoxic properties in vitro. We continue here our exploratory analysis through the lens of metabolomics to identify potentially altered metabolites and biological pathways. Cell extracts from neurotoxic and control astrocytes were compared using high-resolution mass spectrometrybased metabolomics. Around 12 % of metabolic features demonstrated significant differences between neurotoxic and control astrocytes, including alterations in the key metabolite glutamate. Consistent with our previous transcriptomic study, the present results illustrate many homeostatic and regulatory functions of metabolites, suggesting that neurotoxic 3xTg-AD astrocytes exhibit alterations in the Krebs cycle as well as the prostaglandin pathway.This is the first metabolomic study performed in 3xTg-AD neurotoxic astrocytes. These results provide insight into metabolic alterations potentially associated with neurotoxicity and pathology progression in the 3xTg-AD mouse model and strengthen the therapeutic potential of astrocytes in AD. Biological significance: Our study is the first high-resolution metabolomic characterization of the novel neurotoxic 3xTg-AD astrocytes. We propose key metabolites and pathway alterations, as well as possible associations with gene expression alterations in the model. Our results are in line with recent hypotheses beyond the amyloid cascade, considering the involvement of several stress response cascades during the development of Alzheimer’s disease. This work could inspire other researchers to initiate similar studies in related models. Furthermore, this work illustrates a powerful workflow for metabolite annotation and selection that can be implemented in other studies.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[<strong>Carvalho, Diego</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Díaz Amarilla, Pablo</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Smith, Mathew R.</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Santi, María Daniela</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Martinez-Busi, Marcela</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Go, Young-Mi</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Jones, Dean P.</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Duarte, Pablo</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Savio, Eduardo</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Abin-Carriquiry, Juan A.</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Arredondo Unanua, María Florencia</strong>]]></dcterms:creator>
    <dcterms:source><![CDATA[Journal of Proteomics, v.310, 2025. -- e105336]]></dcterms:source>
    <dcterms:publisher><![CDATA[Elsevier]]></dcterms:publisher>
    <dcterms:date><![CDATA[2025]]></dcterms:date>
    <dcterms:rights><![CDATA[<div class="element-text">
<p><strong>Información sobre Derechos de Autor</strong></p>
<p>(Por favor lea este aviso antes de abrir los documentos u objetos)</p>
<p><strong>La legislación uruguaya protege el derecho</strong> de autor sobre toda creación literaria, científica o artística, tanto en lo que tiene que ver con sus derechos morales, como en lo referente a los derechos patrimoniales con sujeción a lo establecido por el derecho común y las siguientes leyes (LEY 9.739 DE 17 DE DICIEMBRE DE 1937 SOBRE PROPIEDAD LITERARIA Y ARTISTICA CON LAS MODIFICACIONES INTRODUCIDAS POR LA LEY DE DERECHO DE AUTOR Y DERECHOS CONEXOS No. 17.616 DE 10 DE ENERO DE 2003, LEY 17.805 DE 26 DE AGOSTO DE 2004, LEY 18.046 DE 24 DE OCTUBRE DE 2006 LEY 18.046 DE 24 DE OCTUBRE DE 2006)</p>
<p><strong>ADVERTENCIA -</strong> La consulta de este documento queda condicionada a la aceptación de las siguientes condiciones de uso: Este documento es únicamente para usos privados enmarcados en actividades de investigación y docencia. No se autoriza su reproducción con fines de lucro. Esta reserva de derechos afecta tanto los datos del documento como a sus contenidos. En la utilización o cita de partes debe indicarse el nombre de la persona autora.</p>
</div>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:extent><![CDATA[11 p.]]></dcterms:extent>
    <dcterms:language><![CDATA[Inglés]]></dcterms:language>
    <dcterms:type><![CDATA[Artículo]]></dcterms:type>
    <dcterms:identifier><![CDATA[10.1016/j.jprot.2024.105336]]></dcterms:identifier>
</rdf:Description><rdf:Description rdf:about="https://riquim.fq.edu.uy/items/show/5175">
    <dcterms:title><![CDATA[<strong>Aggressive mutation in a familial adenomatous polyposis syndrome family : when phenotype guides clinical surveillance</strong>]]></dcterms:title>
    <dcterms:subject><![CDATA[FENOTIPO]]></dcterms:subject>
    <dcterms:subject><![CDATA[POLIPOSIS ADENOMATOSA FAMILIAR]]></dcterms:subject>
    <dcterms:subject><![CDATA[BIBLIOGRAFIA NACIONAL QUIMICA]]></dcterms:subject>
    <dcterms:subject><![CDATA[2018]]></dcterms:subject>
    <dcterms:abstract><![CDATA[Familial adenomatous polyposis (FAP) is an autosomal dominant genetic condition, caused by mutations in the adenomatous polyposis coli (APC) tumor suppressor gene. Desmoid tumors (DTs) are seen in 15% to 20% of FAP patients. Specific location of mutation serves as a guide to predict colonic and extra colonic manifestations and their aggressiveness. A severe FAP-phenotypic family was registered in a genetic counselling high-risk Uruguayan hereditary cancer clinic. Proband&rsquo;s DNA was analysed by NGS, detecting a pathogenic mutation in APC gene. All willing family members were counselled and encouraged to be tested. Here we report a kindred formed by 16 individuals with a very severe FAP phenotype. A two-base deletion mutation: c.4393_4394delAG in APC gene and a consequent premature stop codon was detected. DTs were diagnosed in 6 individuals, ranging from 2 to 25 years of age. The causes of death were diverse: gastric cancer, rectal cancer and desmoid tumor. The already described genotype-phenotype correlation has proved its worth in this family, as clinical features reflect the mutation location at 3&rsquo; end of APC gene. The inheritable and lethal nature of the disease needs a tailored follow up approach in order to reduce mortality, optimize local tumor control, and preserve patients&rsquo; quality of life.]]></dcterms:abstract>
    <dcterms:creator><![CDATA[<strong>Neffa, Florencia</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Garc&iacute;a, Luc&iacute;a</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Della Valle, Adriana</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Carusso, Florencia</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Vergara, Carolina</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Sanchez, Daniel</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Sapone, Marta</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Sylveira, Noelia</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<strong>Revello, Ana Laura</strong>]]></dcterms:creator>
    <dcterms:creator><![CDATA[<a title="Curriculum Vitae" href="http://buscadores.anii.org.uy/buscador_sni/exportador/ExportarPdf?hash=8b87e8e50f3fa6cbb61ecc6edf70e6f8" target="_self"><strong>Esper&oacute;n, Patricia</strong></a>]]></dcterms:creator>
    <dcterms:source><![CDATA[Journal of Gastrointestinal Oncology&nbsp; v.8, no. 9, 2018. -- p. 553-559]]></dcterms:source>
    <dcterms:publisher><![CDATA[AME]]></dcterms:publisher>
    <dcterms:date><![CDATA[2018]]></dcterms:date>
    <dcterms:rights><![CDATA[<p><strong>Informaci&oacute;n sobre Derechos de Autor</strong></p>
<p>(Por favor lea este aviso antes de abrir los documentos u objetos)</p>
<p><strong> La legislaci&oacute;n uruguaya protege el derecho</strong> de autor sobre toda creaci&oacute;n literaria, cient&iacute;fica o art&iacute;stica, tanto en lo que tiene que ver con sus derechos morales, como en lo referente a los derechos patrimoniales con sujeci&oacute;n a lo establecido por el derecho com&uacute;n y las siguientes leyes (LEY 9.739 DE 17 DE DICIEMBRE DE 1937 SOBRE PROPIEDAD LITERARIA Y ARTISTICA CON LAS MODIFICACIONES INTRODUCIDAS POR LA LEY DE DERECHO DE AUTOR Y DERECHOS CONEXOS No. 17.616 DE 10 DE ENERO DE 2003, LEY 17.805 DE 26 DE AGOSTO DE 2004, LEY 18.046 DE 24 DE OCTUBRE DE 2006)</p>
<p><strong> ADVERTENCIA -</strong> La consulta de este documento queda condicionada a la aceptaci&oacute;n de las siguientes condiciones de uso: Este documento es &uacute;nicamente para usos privados enmarcados en actividades de investigaci&oacute;n y docencia. No se autoriza su reproducci&oacute;n con fines de lucro. Esta reserva de derechos afecta tanto los datos del documento como a sus contenidos. En la utilizaci&oacute;n o cita de partes debe indicarse el nombre de la persona autora.</p>]]></dcterms:rights>
    <dcterms:format><![CDATA[PDF]]></dcterms:format>
    <dcterms:language><![CDATA[Ingl&eacute;s]]></dcterms:language>
    <dcterms:type><![CDATA[Art&iacute;culo]]></dcterms:type>
    <dcterms:identifier><![CDATA[DOI:: 10.21037/jgo.2018.06.10]]></dcterms:identifier>
</rdf:Description></rdf:RDF>
