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                  <text>Bibliografía Nacional Química</text>
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                  <text>Contiene la producción científica nacional de los profesionales químicos e investigadores, durante el período 1929 hasta la fecha.</text>
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                <text>&lt;strong&gt;Untargeted metabolomics of 3xTg-AD neurotoxic astrocytes&lt;/strong&gt;</text>
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                <text>ENFERMEDAD DE ALZHEIMER</text>
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                <text>RATONES 3x-Tg-AD</text>
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                <text>DEMENCIA</text>
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                <text>BIBLIOGRAFIA NACIONAL QUIMICA</text>
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                <text>2025</text>
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                <text>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.</text>
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                <text>&lt;strong&gt;Carvalho, Diego&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Díaz Amarilla, Pablo&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Smith, Mathew R.&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Santi, María Daniela&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Martinez-Busi, Marcela&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Go, Young-Mi&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Jones, Dean P.&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Duarte, Pablo&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Savio, Eduardo&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Abin-Carriquiry, Juan A.&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Arredondo Unanua, María Florencia&lt;/strong&gt;</text>
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                <text>Journal of Proteomics, v.310, 2025. -- e105336</text>
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                <text>Elsevier</text>
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                <text>2025</text>
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&lt;p&gt;&lt;strong&gt;Información sobre Derechos de Autor&lt;/strong&gt;&lt;/p&gt;
&lt;p&gt;(Por favor lea este aviso antes de abrir los documentos u objetos)&lt;/p&gt;
&lt;p&gt;&lt;strong&gt;La legislación uruguaya protege el derecho&lt;/strong&gt; 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)&lt;/p&gt;
&lt;p&gt;&lt;strong&gt;ADVERTENCIA -&lt;/strong&gt; 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.&lt;/p&gt;
&lt;/div&gt;</text>
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            <description>The size or duration of the resource.</description>
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                <text>11 p.</text>
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            <description>A language of the resource</description>
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                <text>10.1016/j.jprot.2024.105336</text>
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        <name>Astrocitos</name>
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        <name>Demencia</name>
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        <name>Enfermedad de Alzheimer</name>
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        <name>Enfermedades neuromusculares</name>
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        <name>Fenotipo</name>
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        <name>Flavonoides</name>
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        <name>Metabolómica</name>
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        <name>Ratones 3x-Tg-AD</name>
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        <name>Sistema nervioso</name>
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              <name>Title</name>
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                  <text>Bibliografía Nacional Química</text>
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              <description>An account of the resource</description>
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                <elementText elementTextId="709198">
                  <text>Contiene la producción científica nacional de los profesionales químicos e investigadores, durante el período 1929 hasta la fecha.</text>
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                <elementText elementTextId="709199">
                  <text>Departamento de Documentación y Biblioteca</text>
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                  <text>RIQUIM</text>
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          <description>If the image is of an object, state the type of object, such as painting, sculpture, paper, photo, and additional data</description>
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                <text>&lt;strong&gt;Prenatal exposure to vaporized high-potency cannabis affects hippocampal synaptic remodeling and efficacy, axonal excitability, and memory in offspring&lt;/strong&gt;</text>
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                <text>CANNABIS SATIVA</text>
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                <text>EMBARAZO</text>
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                <text>CANNABINOIDES</text>
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                <text>NEURODESARROLLO</text>
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                <text>SISTEMA NERVIOSO</text>
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                <text>DESARROLLO EMBRIONARIO</text>
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                <text>TRASTORNOS RELACIONADOS CON SUSTANCIAS</text>
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                <text>MEMORIA</text>
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                <text>EXCITABILIDAD NEURONAL</text>
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                <text>FUNCION SINAPTICA</text>
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                <text>BIBLIOGRAFIA NACIONAL QUIMICA</text>
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                <text>2025</text>
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            <description>A summary of the resource.</description>
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                <text>Cannabis use during pregnancy has recently become an important concern due to its increasing trend and association with neurodevelopmental alterations of exposed children. Although inhalation is the primary route of cannabis consumption in humans, few studies replicated this route in preclinical models of prenatal exposure. This study aimed to analyze the effects of chronic prenatal exposure to vaporized cannabis (PEVC) on hippocampal neurodevelopment, functionality, and learning and memory processes. Using a commercially available high-potency cannabis strain (THC 14.7%), pregnant rats were exposed to cannabis vapor from gestational day 8 to 21. A combination of primary hippocampal cultures, electrophysiological studies in slices, and behavioral tests was employed to assess the impact of PEVC. We found that PEVC induced presynaptic remodeling of hippocampal neurons in offspring under both basal and activity-dependent conditions by increasing synaptic vGlut1 abundance and the total recycling pool of synaptic vesicles. Chronic PEVC also induced a downregulation of CB1R at glutamatergic and GABAergic synapses. Additionally, an increase in axonal recruitment and synaptic efficacy was observed at hippocampal CA1 synapses of juvenile offspring. Moreover, long-lasting cognitive impairments were identified during adolescence, including deficits in spatial memory in male and female offspring. In summary, these findings demonstrate that exposure to high-potency cannabis vapor during pregnancy leads to significant changes in synaptic remodeling and efficacy, axonal recruitment, and long-term cognitive consequences in offspring.</text>
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            <description>An entity primarily responsible for making the resource</description>
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                <text>&lt;strong&gt;Cairus, Andrea&lt;/strong&gt;</text>
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                <text>&lt;a href="https://export.cvuy.uy/cv/?38d528d1650d2bdddaceb4a5c518df7a"&gt;&lt;strong&gt;Brizolara, Facundo&lt;/strong&gt;&lt;/a&gt;</text>
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                <text>&lt;strong&gt;Kunizawa, Héctor&lt;/strong&gt;</text>
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                <text>&lt;a href="https://export.cvuy.uy/cv/?7ea21656fc488a603c8b6b48d587a610"&gt;&lt;strong&gt;Clouzet, Vanina&lt;/strong&gt;&lt;/a&gt;</text>
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                <text>&lt;strong&gt;Gonzalez, Giuliana&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Alsina-Llanes, Marcela&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Dellepiane, Lucía&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;Fernández, Santiago&lt;/strong&gt;</text>
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                <text>&lt;strong&gt;García-Carnelli, Carlos&lt;/strong&gt;</text>
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                <text>&lt;a href="https://export.cvuy.uy/cv/?95d73eb1f1d4ebab44f3a518a40237b744eb19f3b78ed07bf4908d1191e026088c62692d4bc22ce64fd7d20931f0ecc4e9ddcc92a24d0560d36b960129dd00cf"&gt;&lt;strong&gt;Umpierrez, Eleuterio&lt;/strong&gt;&lt;/a&gt;</text>
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                <text>&lt;a href="https://export.cvuy.uy/cv/?08c4f196451d3f432a40a0d4d071777e76d44e72847ab75eb3519ac68a255b90c6c33f816e231a527710d67f5098b09206a3af64758ffb6ac1aa749ff6ca02a0"&gt;&lt;strong&gt;Borde Bebeacua, Michel&lt;/strong&gt;&lt;/a&gt;</text>
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                <text>&lt;a href="https://export.cvuy.uy/cv/?340492469d89c484d52055c12af87b8c35718ea61ba1203c39c181368a7d6b1d58feada0dbc6e52a069c2f4423dbcdad9c87e6ef38191b32c27f6cfdcd339420"&gt;&lt;strong&gt;Prieto, José Pedro&lt;/strong&gt;&lt;/a&gt;</text>
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                <text>&lt;a href="https://export.cvuy.uy/cv/?5003e5073c74bf11eafd062afbedf3535450db79f0f13ac99f69e42c026831c27a42da885ab02e544ec837daaf0f0274881f745534f6dfd4ef47232fe5c5e623"&gt;&lt;strong&gt;Vitureira Serpa, Nathalia&lt;/strong&gt;&lt;/a&gt;</text>
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            <description>A related resource from which the described resource is derived</description>
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              <elementText elementTextId="709992">
                <text>Journal of Neurochemistry, v. 169, n°7, 2025. -- e70153</text>
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            <name>Publisher</name>
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              <elementText elementTextId="709993">
                <text>Wiley</text>
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            <description>A point or period of time associated with an event in the lifecycle of the resource</description>
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              <elementText elementTextId="709994">
                <text>2025</text>
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            <description>Information about rights held in and over the resource</description>
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&lt;p&gt;&lt;strong&gt;Información sobre Derechos de Autor&lt;/strong&gt;&lt;/p&gt;
&lt;p&gt;(Por favor lea este aviso antes de abrir los documentos u objetos)&lt;/p&gt;
&lt;p&gt;&lt;strong&gt;La legislación uruguaya protege el derecho&lt;/strong&gt; 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)&lt;/p&gt;
&lt;p&gt;&lt;strong&gt;ADVERTENCIA -&lt;/strong&gt; 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.&lt;/p&gt;
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