<?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>2026-06-27T10:21:25Z</responseDate><request verb="GetRecord" identifier="oai:docta.ucm.es:20.500.14352/115652" metadataPrefix="mods">https://docta.ucm.es/rest/oai/request</request><GetRecord><record><header><identifier>oai:docta.ucm.es:20.500.14352/115652</identifier><datestamp>2025-08-26T13:02:29Z</datestamp><setSpec>com_20.500.14352_14</setSpec><setSpec>col_20.500.14352_15</setSpec></header><metadata><mods:mods xmlns:mods="http://www.loc.gov/mods/v3" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xmlns:doc="http://www.lyncode.com/xoai" xsi:schemaLocation="http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-1.xsd">
   <mods:name>
      <mods:namePart>Cediel, R</mods:namePart>
   </mods:name>
   <mods:name>
      <mods:namePart>Contreras, J</mods:namePart>
   </mods:name>
   <mods:name>
      <mods:namePart>Murillo-Cuesta, S</mods:namePart>
   </mods:name>
   <mods:name>
      <mods:namePart>Hernandez-Sanchez, C</mods:namePart>
   </mods:name>
   <mods:name>
      <mods:namePart>Cerdan, S</mods:namePart>
   </mods:name>
   <mods:name>
      <mods:namePart>Varela-Nieto, I</mods:namePart>
   </mods:name>
   <mods:name>
      <mods:namePart>Riquelme Arias, Gerardo</mods:namePart>
   </mods:name>
   <mods:name>
      <mods:namePart>Rodríguez De La Rosa, José Carlos</mods:namePart>
   </mods:name>
   <mods:name>
      <mods:namePart>Hernández Sánchez, Lucía</mods:namePart>
   </mods:name>
   <mods:name>
      <mods:namePart>Zubeldia Ortuño, José Manuel</mods:namePart>
   </mods:name>
   <mods:extension>
      <mods:dateAvailable encoding="iso8601">2025-01-22T16:33:58Z</mods:dateAvailable>
   </mods:extension>
   <mods:extension>
      <mods:dateAccessioned encoding="iso8601">2025-01-22T16:33:58Z</mods:dateAccessioned>
   </mods:extension>
   <mods:originInfo>
      <mods:dateIssued encoding="iso8601">2010</mods:dateIssued>
   </mods:originInfo>
   <mods:identifier type="doi">10.3389/fnana.2010.00027</mods:identifier>
   <mods:identifier type="uri">https://hdl.handle.net/20.500.14352/115652</mods:identifier>
   <mods:identifier type="officialurl">https://doi.org/10.3389/fnana.2010.00027</mods:identifier>
   <mods:identifier type="relatedurl">https://www.frontiersin.org/journals/neuroanatomy/articles/10.3389/fnana.2010.00027/full</mods:identifier>
   <mods:abstract>Insulin-like growth factor-I (IGF-I) belongs to the family of insulin-related peptides that fulfils a key role during the late development of the nervous system. Human IGF1 mutations cause profound deafness, poor growth and mental retardation. Accordingly, Igf1(-/-) null mice are dwarfs that have low survival rates, cochlear alterations and severe sensorineural deafness. Presbycusis (age-related hearing loss) is a common disorder associated with aging that causes social and cognitive problems. Aging is also associated with a decrease in circulating IGF-I levels and this reduction has been related to cognitive and brain alterations, although there is no information as yet regarding the relationship between presbycusis and IGF-I biodisponibility. Here we present a longitudinal study of wild type Igf1(+/+) and null Igf1(-/-) mice from 2 to 12 months of age comparing the temporal progression of several parameters: hearing, brain morphology, cochlear cytoarchitecture, insulin-related factors and IGF gene expression and IGF-I serum levels. Complementary invasive and non-invasive techniques were used, including auditory brainstem-evoked response (ABR) recordings and in vivo MRI brain imaging. Igf1(-/-) null mice presented profound deafness at all the ages studied, without any obvious worsening of hearing parameters with aging. Igf1(+/+) wild type mice suffered significant age-related hearing loss, their auditory thresholds and peak I latencies augmenting as they aged, in parallel with a decrease in the circulating levels of IGF-I. Accordingly, there was an age-related spiral ganglion degeneration in wild type mice that was not evident in the Igf1 null mice. However, the Igf1(-/-) null mice in turn developed a prematurely aged stria vascularis reminiscent of the diabetic strial phenotype. Our data indicate that IGF-I is required for the correct development and maintenance of hearing, supporting the idea that IGF-I-based therapies could contribute to prevent or ameliorate age-related hearing loss.</mods:abstract>
   <mods:language>
      <mods:languageTerm>eng</mods:languageTerm>
   </mods:language>
   <mods:accessCondition type="useAndReproduction">http://creativecommons.org/licenses/by-nc-nd/4.0/</mods:accessCondition>
   <mods:accessCondition type="useAndReproduction">open access</mods:accessCondition>
   <mods:accessCondition type="useAndReproduction">Attribution-NonCommercial-NoDerivatives 4.0 International</mods:accessCondition>
   <mods:titleInfo>
      <mods:title>A comparative study of age-related hearing loss in wild type and insulin-like growth factor I deficient mice</mods:title>
   </mods:titleInfo>
   <mods:genre>journal article</mods:genre>
</mods:mods></metadata></record></GetRecord></OAI-PMH>