<?xml version="1.0" encoding="UTF-8"?><?xml-stylesheet type="text/xsl" href="static/style.xsl"?><OAI-PMH xmlns="http://www.openarchives.org/OAI/2.0/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/ http://www.openarchives.org/OAI/2.0/OAI-PMH.xsd"><responseDate>2026-06-04T05:44:50Z</responseDate><request verb="GetRecord" identifier="oai:riuma.uma.es:10630/24853" metadataPrefix="rdf">https://riuma.uma.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:riuma.uma.es:10630/24853</identifier><datestamp>2026-03-13T07:35:14Z</datestamp><setSpec>com_10630_2254</setSpec><setSpec>col_10630_37959</setSpec></header><metadata><rdf:RDF xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns:doc="http://www.lyncode.com/xoai" xmlns:ds="http://dspace.org/ds/elements/1.1/" xmlns:ow="http://www.ontoweb.org/ontology/1#" xmlns:rdf="http://www.openarchives.org/OAI/2.0/rdf/" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xsi:schemaLocation="http://www.openarchives.org/OAI/2.0/rdf/ http://www.openarchives.org/OAI/2.0/rdf.xsd">
   <ow:Publication rdf:about="oai:riuma.uma.es:10630/24853">
      <dc:title>WAT alterations in diabetic mice: its connection and implication in ad pathogenesis.</dc:title>
      <dc:creator>Bettinetti-Luque, Miriam</dc:creator>
      <dc:creator>Trujillo-Estrada, Laura Isabel</dc:creator>
      <dc:creator>Andreo-López, Juana</dc:creator>
      <dc:creator>Cantero-Molina, Francisco</dc:creator>
      <dc:creator>Da Cunha, Celia</dc:creator>
      <dc:creator>Sánchez-Mejías, Elisabeth</dc:creator>
      <dc:creator>LaFerla, Frank</dc:creator>
      <dc:creator>Gutiérrez-Pérez, Antonia</dc:creator>
      <dc:creator>Baglietto-Vargas, David</dc:creator>
      <dc:creator>Baglietto-Vargas, David</dc:creator>
      <dc:description>Alzheimer’s disease (AD) is a complex disorder and multiple cellular and molecular mechanisms are involved in AD onset&#xd;
and progression. Recent evidences have suggested that metabolic alterations are an important pathological feature in&#xd;
disease progression in AD. Likewise, diabetes and obesity, two mayor metabolic illnesses associated with white adipose&#xd;
tissue expansion, are risk factors for AD. Here, we hypothesize that the white adipose tissue may serve as a key communicator organ between the brain and peripheral metabolic illnesses. We used histological stains,&#xd;
immunohistochemistry and biochemical means to determine changes in the white adipose tissue from WT and db/db mice.&#xd;
Moreover, similar techniques were used in the brain of 3xTg-AD mice that received white fat pads from WT and db/db donors to determine any changes in amyloid and tau pathology. Our study shows that recipient 3xTg-AD mice from db/db fat pads mice develop profound changes in tau pathology due to increased CDK5/p25 expression compared to 3xTg-AD mice that&#xd;
received fad pads from WT mice. This increment in tau level was associated with elevated levels in IL-1β and microglial activation. However, we found that Aβ levels were reduced in recipient 3xTg-AD mice from db/db fat pads compared to 3xTg-&#xd;
AD mice that received fad pads from WT mice. These reduction in Aβ levels were correlated with an increment in microglia&#xd;
phagocytic capacity. Overall, our study demonstrates a novel important crosstalk between AD and diabetes type II through white adipose cells and a differential effect on tau and Aβ pathology.</dc:description>
      <dc:date>2022-08-31T10:43:59Z</dc:date>
      <dc:date>2022-08-31T10:43:59Z</dc:date>
      <dc:date>2022-07-13</dc:date>
      <dc:type>conference output</dc:type>
      <dc:identifier>https://hdl.handle.net/10630/24853</dc:identifier>
      <dc:language>eng</dc:language>
      <dc:relation>FENS Forum 2022</dc:relation>
      <dc:relation>París, Francia</dc:relation>
      <dc:relation>9-13 de Julio</dc:relation>
      <dc:rights>http://creativecommons.org/licenses/by-nc-nd/4.0/</dc:rights>
      <dc:rights>open access</dc:rights>
      <dc:rights>Attribution-NonCommercial-NoDerivatives 4.0 Internacional</dc:rights>
   </ow:Publication>
</rdf:RDF>
</metadata></record></GetRecord></OAI-PMH>