<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>14</volume><submitter>Holden S</submitter><funding>Office of Extramural Research, National Institutes of Health</funding><pubmed_abstract>Mice expressing human amyloid precursor protein (APP) containing the dominant Swedish and Iberian mutations (&lt;i>App&lt;sup>NL-F&lt;/sup>&lt;/i> ) or also Arctic mutation (&lt;i>App&lt;sup>NL-G-F&lt;/sup>&lt;/i> ) show neuropathology and hippocampus-dependent cognitive impairments pertinent to Alzheimer's disease (AD) in mouse models at 18 and 6 months of age, respectively. Apolipoprotein E, involved in cholesterol metabolism, plays an important role in maintaining the brain. There are three human apolipoprotein E isoforms: E2, E3, and E4. Compared to E3, E4 increases while E2 protects against AD risk. At 6 months of age, prior to the onset of plaque pathology, E3, but not E4, protected against hAPP/Aβ-induced impairments in spatial memory retention in the Morris water maze. However, these earlier studies were </pubmed_abstract><journal>Frontiers in aging neuroscience</journal><pagination>767558</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8922030</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Apolipoprotein E Isoform-Dependent Effects on Human Amyloid Precursor Protein/Aβ-Induced Behavioral Alterations and Cognitive Impairments and Insoluble Cortical Aβ42 Levels.</pubmed_title><pmcid>PMC8922030</pmcid><pubmed_authors>Torres ERS</pubmed_authors><pubmed_authors>Krenik D</pubmed_authors><pubmed_authors>Turker MS</pubmed_authors><pubmed_authors>Kundu P</pubmed_authors><pubmed_authors>Raber J</pubmed_authors><pubmed_authors>Sudhakar R</pubmed_authors><pubmed_authors>Grygoryev D</pubmed_authors><pubmed_authors>Holden S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Apolipoprotein E Isoform-Dependent Effects on Human Amyloid Precursor Protein/Aβ-Induced Behavioral Alterations and Cognitive Impairments and Insoluble Cortical Aβ42 Levels.</name><description>Mice expressing human amyloid precursor protein (APP) containing the dominant Swedish and Iberian mutations (&lt;i>App&lt;sup>NL-F&lt;/sup>&lt;/i> ) or also Arctic mutation (&lt;i>App&lt;sup>NL-G-F&lt;/sup>&lt;/i> ) show neuropathology and hippocampus-dependent cognitive impairments pertinent to Alzheimer's disease (AD) in mouse models at 18 and 6 months of age, respectively. Apolipoprotein E, involved in cholesterol metabolism, plays an important role in maintaining the brain. There are three human apolipoprotein E isoforms: E2, E3, and E4. Compared to E3, E4 increases while E2 protects against AD risk. At 6 months of age, prior to the onset of plaque pathology, E3, but not E4, protected against hAPP/Aβ-induced impairments in spatial memory retention in the Morris water maze. However, these earlier studies were </description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-29T11:03:32.505Z</modification><creation>2025-04-06T19:47:50.823Z</creation></dates><accession>S-EPMC8922030</accession><cross_references><pubmed>35299942</pubmed><doi>10.3389/fnagi.2022.767558</doi></cross_references></HashMap>