<?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>1665-5044</journal-id>
<journal-title><![CDATA[Revista mexicana de neurociencia]]></journal-title>
<abbrev-journal-title><![CDATA[Rev. mex. neurocienc.]]></abbrev-journal-title>
<issn>1665-5044</issn>
<publisher>
<publisher-name><![CDATA[Academia Mexicana de Neurología A.C.]]></publisher-name>
</publisher>
</journal-meta>
<article-meta>
<article-id>S1665-50442021000500184</article-id>
<article-id pub-id-type="doi">10.24875/rmn.20000087</article-id>
<title-group>
<article-title xml:lang="en"><![CDATA[Alterations in diabetes mellitus gene expression in the development and progression of Alzheimer's disease: The PI3K/Akt pathway link]]></article-title>
<article-title xml:lang="es"><![CDATA[Alteraciones de la expresión génica de la diabetes mellitus en el desarrollo y progresión de la enfermedad de Alzheimer: el vínculo de la vía PI3K/Akt]]></article-title>
</title-group>
<contrib-group>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Hernández-Contreras]]></surname>
<given-names><![CDATA[Karla A.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Hernández-Aguilar]]></surname>
<given-names><![CDATA[María Elena]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Herrera-Covarrubias]]></surname>
<given-names><![CDATA[Deissy]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Rojas-Durán]]></surname>
<given-names><![CDATA[Fausto]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
<contrib contrib-type="author">
<name>
<surname><![CDATA[Aranda-Abreu]]></surname>
<given-names><![CDATA[Gonzalo E.]]></given-names>
</name>
<xref ref-type="aff" rid="Aff"/>
</contrib>
</contrib-group>
<aff id="Af1">
<institution><![CDATA[,Universidad Veracruzana Instituto de Investigaciones Cerebrales ]]></institution>
<addr-line><![CDATA[Xalapa ]]></addr-line>
<country>Mexico</country>
</aff>
<pub-date pub-type="pub">
<day>00</day>
<month>10</month>
<year>2021</year>
</pub-date>
<pub-date pub-type="epub">
<day>00</day>
<month>10</month>
<year>2021</year>
</pub-date>
<volume>22</volume>
<numero>5</numero>
<fpage>184</fpage>
<lpage>195</lpage>
<copyright-statement/>
<copyright-year/>
<self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_arttext&amp;pid=S1665-50442021000500184&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_abstract&amp;pid=S1665-50442021000500184&amp;lng=en&amp;nrm=iso"></self-uri><self-uri xlink:href="http://www.scielo.org.mx/scielo.php?script=sci_pdf&amp;pid=S1665-50442021000500184&amp;lng=en&amp;nrm=iso"></self-uri><abstract abstract-type="short" xml:lang="en"><p><![CDATA[Abstract Considered a neurodegenerative disease, Alzheimer's disease (AD) involves a physiopathological process characterized by the presence of the beta-amyloid peptide, hyperphosphorylated Tau protein, and neuroinflammation. Diabetes mellitus (DM) is an endocrine disease characterized by insulin resistance, where decreased production of this hormone causes a constant state of hyperglycemia. Although it is recognized that DM is a risk factor for the development of AD, the compression of the mechanisms involved is not completely understood. The present review evaluates the information acquired from primary and secondary sources, focusing on the alterations in gene expression associated with AD as well as the alterations in gene expression associated with DM, to later highlight the influence that these types of alterations developed in patients with DM can have on both the development and progression of AD. Finally, we point out those alterations that impact the phosphatidyl Inositol 3 Kinase/Akt (PI3K/Akt) pathway, which seems to intervene in the physiopathological process of both diseases, considering that the compression of these gene alterations can help us understand the intricate link between DM and AD.]]></p></abstract>
<abstract abstract-type="short" xml:lang="es"><p><![CDATA[Resumen Considerada una enfermedad neurodegenerativa, la enfermedad de Alzheimer (EA) implica un proceso fisiopatológico caracterizado por la presencia del péptido beta amiloide, la proteína Tau hiperfosforilada y la neuroinflamación. La diabetes mellitus (DM) es una enfermedad endocrina caracterizada por la resistencia a la insulina, donde la disminución de la producción de esta hormona causa un estado constante de hiperglucemia. Aunque se reconoce que la DM es un factor de riesgo para el desarrollo de la EA, la compresión de los mecanismos involucrados no se comprende completamente. En el presente trabajo se evalúa la información adquirida de fuentes primarias y secundarias, centrándose en las alteraciones de la expresión génica asociadas a la EA, así como en las alteraciones de la expresión génica asociadas a la DM, para posteriormente destacar la influencia que este tipo de alteraciones desarrolladas en pacientes con DM pueden tener tanto en el desarrollo como en la progresión de la EA. Por último, señalamos aquellas alteraciones que inciden en la vía del fosfatidilinositol-3-quinasa/Akt (PI3K/Akt), que parece intervenir en el proceso fisiopatológico de ambas enfermedades, considerando que la compresión de estas alteraciones genéticas puede ayudarnos a entender el intrincado vínculo entre la DM y la EA.]]></p></abstract>
<kwd-group>
<kwd lng="en"><![CDATA[Alzheimer's disease]]></kwd>
<kwd lng="en"><![CDATA[Diabetes mellitus]]></kwd>
<kwd lng="en"><![CDATA[Akt pathway]]></kwd>
<kwd lng="es"><![CDATA[Enfermedad de Alzheimer]]></kwd>
<kwd lng="es"><![CDATA[Diabetes mellitus]]></kwd>
<kwd lng="es"><![CDATA[Vía de Akt]]></kwd>
</kwd-group>
</article-meta>
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