<?xml version="1.0" encoding="ISO-8859-1"?><article xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance">
<front>
<journal-meta>
<journal-id>0120-8748</journal-id>
<journal-title><![CDATA[Acta Neurológica Colombiana]]></journal-title>
<abbrev-journal-title><![CDATA[Acta Neurol Colomb.]]></abbrev-journal-title>
<issn>0120-8748</issn>
<publisher>
<publisher-name><![CDATA[Asociación Colombiana de Neurología]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S0120-87482024000300005</article-id>
<article-id pub-id-type="doi">10.22379/anc.v40i3.1341</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Depresión, ansiedad y microbiota intestinal: mecanismos neurobiológicos]]></article-title>
<article-title xml:lang="en"><![CDATA[Depression, anxiety, and intestinal microbiota: Neurobiological mechanisms]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Sabine Kransel]]></surname>
<given-names><![CDATA[Marah Sophie]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Jaramillo Zafra]]></surname>
<given-names><![CDATA[Juan Jose]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Osorio Diago]]></surname>
<given-names><![CDATA[Isabella]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Becerra Hernández]]></surname>
<given-names><![CDATA[Lina Vanessa]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Pontificia Universidad Javeriana  ]]></institution>
<addr-line><![CDATA[Cali ]]></addr-line>
<country>Colombia</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Pontificia Universidad Javeriana Departamento de Ciencias Básicas de la Salud ]]></institution>
<addr-line><![CDATA[Cali ]]></addr-line>
<country>Colombia</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>09</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>09</month>
<year>2024</year>
</pub-date>
<volume>40</volume>
<numero>3</numero>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_arttext&amp;pid=S0120-87482024000300005&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_abstract&amp;pid=S0120-87482024000300005&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.co/scielo.php?script=sci_pdf&amp;pid=S0120-87482024000300005&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen  Introducción: La disbiosis intestinal ha sido reconocida como un factor relevante en la etiología de trastornos neuropsiquiátricos, como la depresión y la ansiedad; aunque la relación entre una microbiota intestinal alterada y estos trastornos está bien documentada, los mecanismos moleculares subyacentes aún no se comprenden completamente. Este estudio revisa la literatura reciente para analizar las vías biológicas que podrían explicar esta conexión.  Materiales y métodos: Se realizó una revisión narrativa de la literatura disponible en bases de datos biomédicas, seleccionando estudios que abordan la relación entre disbiosis intestinal y trastornos afectivos. Se clasificaron los mecanismos implicados en tres categorías: la vía vagal, la permeabilidad intestinal y los efectos de metabolitos bacterianos. Se incluyeron estudios en modelos animales y humanos.  Resultados: La revisión identificó que la disbiosis intestinal afecta al sistema nervioso central a través de tres mecanismos principales: la vía vagal que actúa como un puente entre la microbiota intestinal y el cerebro; la permeabilidad intestinal aumentada que permite la translocación de productos; y los metabolitos bacterianos, como el lipopolisacárido, que inducen neuroinflamación y alteraciones en la neurotransmisión.  Discusión: Los resultados sugieren que la disbiosis intestinal desempeña un papel crucial en la modulación de la inflamación sistémica y cerebral, lo que contribuye a la aparición de síntomas de depresión y ansiedad. La alteración de la barrera intestinal y los efectos de los metabolitos bacterianos son elementos clave en esta relación.  Conclusiones: La disbiosis intestinal y las alteraciones en el eje cerebro-intestino son determinantes en la manifestación de trastornos afectivos, destacando el potencial de la microbiota como objetivo terapéutico en el manejo de la depresión y la ansiedad.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract  Introduction: Gut dysbiosis has been recognized as a relevant factor in the etiology of neuropsychiatry disorders such as depression and anxiety. Although the relationship between altered gut microbiota and these disorders is well documented, the underlying molecular mechanisms remain incompletely understood. This study reviews recent literature to analyze the biological pathways that may explain this connection.  Materials and methods: A narrative review of the available literature was conducted using biomedical databases, selecting studies that address the relationship between gut dysbiosis and affective disorders. The involved mechanisms were classified into three categories: the vagal pathway, intestinal permeability, and the effects of bacterial metabolites. Both animal and human studies were included.  Results: The review identified that gut dysbiosis affects the central nervous system through three main mechanisms: the vagal pathway acts as a bridge between the gut microbiota and the brain, increased intestinal permeability allows the translocation of bacterial products, and bacterial metabolites such as lipopolysaccharides induce neuroinflammation and neurotransmission alterations.  Discussion: The findings suggest that gut dysbiosis plays a critical role in modulating systemic and cerebral inflammation, contributing to the emergence of depressive and anxiety symptoms. Disruption of the intestinal barrier and the effects of bacterial metabolites are key elements in this relationship.  Conclusions: Gut dysbiosis and alterations in the gut-brain axis are key determinants in the manifestation of affective disorders, highlighting the potential of the microbiota as a therapeutic target in managing depression and anxiety.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[ansiedad]]></kwd>
<kwd lng="es"><![CDATA[depresión]]></kwd>
<kwd lng="es"><![CDATA[disbiosis]]></kwd>
<kwd lng="es"><![CDATA[eje cerebro-intestino]]></kwd>
<kwd lng="es"><![CDATA[intestino permeable]]></kwd>
<kwd lng="es"><![CDATA[mecanismos moleculares]]></kwd>
<kwd lng="es"><![CDATA[microbioma intestinal]]></kwd>
<kwd lng="es"><![CDATA[neurobiología]]></kwd>
<kwd lng="en"><![CDATA[Anxiety]]></kwd>
<kwd lng="en"><![CDATA[Depression]]></kwd>
<kwd lng="en"><![CDATA[Dysbiosis]]></kwd>
<kwd lng="en"><![CDATA[Gut-Brain Axis]]></kwd>
<kwd lng="en"><![CDATA[Intestinal microbiome]]></kwd>
<kwd lng="en"><![CDATA[Intestinal permeability]]></kwd>
<kwd lng="en"><![CDATA[Molecular mechanisms]]></kwd>
<kwd lng="en"><![CDATA[Neurobiology]]></kwd>
</kwd-group>
</article-meta>
</front><back>
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