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                  <mods:namePart>Wood, Marcelo</mods:namePart>
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                  <mods:namePart>Green, Kim N.</mods:namePart>
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                  <mods:namePart>LaFerla, Frank M.</mods:namePart>
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                  <mods:namePart>[Baglietto-Vargas,D; Forner,S; Cai,L; Martini,AC; Trujillo-Estrada,L; Swarup,V; Nguyen,MMT; Do Huynh,K; Javonillo,DI; Tran,KM; Phan,J; Kramár,EA; Garcia,F; Childs,J; Rodriguez-Ortiz,CJ; Kitazawa,M; Matheos,DP; Da Cunha,C; Walls,KC; Ager,RR; Tenner,AJ; Wood,M; Green,KM; LaFerla,FM] Institute for Memory Impairments and Neurological Disorders, University of California, Irvine, CA, USA. [Baglietto-Vargas,D; Swarup,V; Kramár,EA; Garcia,F; Childs,J; Tenner,AJ; Wood,M; Green,KM; LaFerla,FM] Department of Neurobiology and Behavior, University of California, Irvine, CA, USA. [Baglietto-Vargas,D; Trujillo-Estrada,L; Nuñez-Diaz,C; Garcia-Leon,JA; Gutierrez,A; Moreno-Gonzalez,I] Department of Cell Biology, Genetic and Physiology, Faculty of Sciences, Instituto de Investigacion Biomedica de Malaga-IBIMA, Networking Research Center on Neurodegenerative Diseases (CIBERNED), University of Malaga, Malaga, Spain. [Jiang,S; Balderrama-Gutierrez,G; Ma,X; Mortazavi,A; MacGregor,GR] Department of Developmental and Cell Biology, University of California, Irvine, CA, USA. [Rodriguez-Ortiz,CJ; Kitazawa,M] Division of Occupational and Environmental Medicine, Department of Medicine. Center for Occupational and Environmental Health (COEH), University of California, Irvine, CA, USA. [Shahnawaz,M; Soto,C; Moreno-Gonzale,I] The Mitchell Center for Alzheimer’s Disease and Related Brain Disorders, Department of Neurology, McGovern Medical School, University of Texas Health Science Center at Houston, Houston, TX, USA. [Tenner,AJ] Department of Molecular Biology and Biochemistry, University of California, Irvine, CA, USA.</mods:namePart>
               </mods:name>
               <mods:extension>
                  <mods:dateAccessioned encoding="iso8601">2024-02-19T15:27:02Z</mods:dateAccessioned>
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                  <mods:dateAvailable encoding="iso8601">2024-02-19T15:27:02Z</mods:dateAvailable>
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               <mods:originInfo>
                  <mods:dateIssued encoding="iso8601">2021-04-23</mods:dateIssued>
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               <mods:identifier type="doi">10.1038/s41467-021-22624-z</mods:identifier>
               <mods:identifier type="e-issn">2041-1723</mods:identifier>
               <mods:identifier type="journal">Nature Communications</mods:identifier>
               <mods:identifier type="other">http://hdl.handle.net/10668/4585</mods:identifier>
               <mods:identifier type="pubmedID">33893290</mods:identifier>
               <mods:identifier type="uri">http://hdl.handle.net/20.500.12105/18320</mods:identifier>
               <mods:abstract>The majority of Alzheimer's disease (AD) cases are late-onset and occur sporadically, however most mouse models of the disease harbor pathogenic mutations, rendering them better representations of familial autosomal-dominant forms of the disease. Here, we generated knock-in mice that express wildtype human Aβ under control of the mouse App locus. Remarkably, changing 3 amino acids in the mouse Aβ sequence to its wild-type human counterpart leads to age-dependent impairments in cognition and synaptic plasticity, brain volumetric changes, inflammatory alterations, the appearance of Periodic Acid-Schiff (PAS) granules and changes in gene expression. In addition, when exon 14 encoding the Aβ sequence was flanked by loxP sites we show that Cre-mediated excision of exon 14 ablates hAβ expression, rescues cognition and reduces the formation of PAS granules.</mods:abstract>
               <mods:language>
                  <mods:languageTerm authority="rfc3066">eng</mods:languageTerm>
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               <mods:accessCondition type="useAndReproduction"/>
               <mods:subject>
                  <mods:topic>Periodic acid-schiff</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Exon</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Cognition</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Mutation</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Gene expression</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Alzheimer disease</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Reacción del ácido peryódico de Schiff</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Exones</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Cognición</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Mutación</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Expresión génica</mods:topic>
               </mods:subject>
               <mods:subject>
                  <mods:topic>Enfermedad de Alzheimer</mods:topic>
               </mods:subject>
               <mods:titleInfo>
                  <mods:title>Generation of a humanized Aβ expressing mouse demonstrating aspects of Alzheimer's disease-like pathology</mods:title>
               </mods:titleInfo>
               <mods:genre>research article</mods:genre>
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