<?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>1870-7203</journal-id>
<journal-title><![CDATA[Acta médica Grupo Ángeles]]></journal-title>
<abbrev-journal-title><![CDATA[Acta méd. Grupo Ángeles]]></abbrev-journal-title>
<issn>1870-7203</issn>
<publisher>
<publisher-name><![CDATA[Grupo Ángeles, Servicios de Salud]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1870-72032024000500392</article-id>
<article-id pub-id-type="doi">10.35366/118817</article-id>
<title-group>
<article-title xml:lang="es"><![CDATA[Atrofia cortical posterior, presentación de un caso]]></article-title>
<article-title xml:lang="en"><![CDATA[Posterior cortical atrophy, a case presentation]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Gómez Ramírez]]></surname>
<given-names><![CDATA[Ana Paola]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Gómez Ramírez]]></surname>
<given-names><![CDATA[Diego Ricardo]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
<xref ref-type="aff" rid="Aaf"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Innes García]]></surname>
<given-names><![CDATA[Ximena]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Márquez Renan]]></surname>
<given-names><![CDATA[Ana]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[González Sánchez]]></surname>
<given-names><![CDATA[Eric Alejandro]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Dorantes Argandar]]></surname>
<given-names><![CDATA[Agustín]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,CINVESTAV Departamento de farmacobiología ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af2">
<institution><![CDATA[,Universidad La Salle Facultad Mexicana de Medicina ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>México</country>
</aff>
<aff id="Af3">
<institution><![CDATA[,Universidad La Salle Facultad Mexicana de Medicina ]]></institution>
<addr-line><![CDATA[ ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>12</month>
<year>2024</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>12</month>
<year>2024</year>
</pub-date>
<volume>22</volume>
<numero>5</numero>
<fpage>392</fpage>
<lpage>398</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1870-72032024000500392&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1870-72032024000500392&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1870-72032024000500392&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen: Se realiza la presentación de un caso de atrofia cortical posterior (ACP), suplementado de una revisión bibliográfica que describe el fenómeno neurodegenerativo que evoluciona a consecuencia de la disminución de tejido neuronal a nivel cortical que se caracteriza por sintomatología que señala una agnosia perceptiva. Los hallazgos fueron enfocados a la alfa-sinucleína (AS) y su papel en la ACP. Los resultados indican que la AS tiene funciones fisiológicas presinápticas, pero su agregación conduce a la formación de fibrillas amiloides, interacción con beta-amiloide y tau, e inclusión neuronal. Esto activa la microglía desencadenando inflamación crónica, estrés oxidativo, así como muerte neuronal. Además, la AS altera mecanismos celulares como la autofagia. En conclusión, la agregación anormal de AS es un factor determinante en la fisiopatología de la ACP, al inducir neurotoxicidad, neuroinflamación, disfunción autofágica y sinergia con otras proteínas alteradas, resultando en atrofia cortical evidente como fue demostrado en la disección del encéfalo.]]></p></abstract>
<abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract: A case of posterior cortical atrophy (ACP) is presented, supplemented by a literature review describing the neurodegenerative phenomenon that evolves due to decreased neuronal tissue at the cortical level, characterized by symptoms indicating perceptual agnosia. The findings focused on alpha-synuclein (AS) and its role in PCA. The results suggest that AS has presynaptic physiological functions, but its aggregation leads to the formation of amyloid fibrils, interaction with beta-amyloid and tau, and neuronal inclusion. This activates microglia, triggering chronic inflammation, oxidative stress, and neuronal death. In addition, AS alters cellular mechanisms such as autophagy. In conclusion, the abnormal aggregation of AS is a determining factor in the pathophysiology of PCA by inducing neurotoxicity, neuroinflammation, autophagic dysfunction, and synergy with other altered proteins, resulting in evident cortical atrophy, as demonstrated in the brain dissection.]]></p></abstract>
<kwd-group>
<kwd lng="es"><![CDATA[alfa-sinucleína]]></kwd>
<kwd lng="es"><![CDATA[beta-amiloide]]></kwd>
<kwd lng="es"><![CDATA[tau]]></kwd>
<kwd lng="es"><![CDATA[atrofia cortical posterior]]></kwd>
<kwd lng="es"><![CDATA[agnosia perceptiva]]></kwd>
<kwd lng="en"><![CDATA[Alpha-synuclein]]></kwd>
<kwd lng="en"><![CDATA[Beta-amyloid]]></kwd>
<kwd lng="en"><![CDATA[tau]]></kwd>
<kwd lng="en"><![CDATA[posterior cortical atrophy]]></kwd>
<kwd lng="en"><![CDATA[perceptual agnosia]]></kwd>
</kwd-group>
</article-meta>
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