<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Anschuetz A</submitter><funding>TauRx Therapeutics Ltd Singapore</funding><pagination>28</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC12838599</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>16(1)</volume><pubmed_abstract>The Icelandic mutation in the amyloid precursor protein (APP), APP&lt;sup>A673T&lt;/sup>, has been identified in Icelandic and Scandinavian populations and is associated with a significantly lower risk of developing Alzheimer's disease (AD). The introduction of the human APP&lt;sup>A673T&lt;/sup> form led to a reduction in amyloid β-protein (Aβ) production and tau pathology, but the effect of mouse APP&lt;sup>A673T&lt;/sup> on tau and Aβ pathology is not well studied. We have crossed line 66 (L66) tau transgenic mice that overexpress the P301S aggregation-prone form of tau with C57Bl6/J mice expressing a single-point mutation edited into the murine &lt;i>APP&lt;/i> gene via CRISPR-Cas gene editing, known as mAPP&lt;sup>A673T&lt;/sup>. We have performed ELISA, histopathological, and behavioural analyses of heterozygous </pubmed_abstract><journal>Biomolecules</journal><pubmed_title>Effect of the Icelandic Mutation APP&lt;sup>A673T&lt;/sup> in the Murine APP Gene on Phenotype of Line 66 Tau Mice.</pubmed_title><pmcid>PMC12838599</pmcid><funding_grant_id>PAR1577 and PAR2074</funding_grant_id><pubmed_authors>Anschuetz A</pubmed_authors><pubmed_authors>Robinson L</pubmed_authors><pubmed_authors>Schwab K</pubmed_authors><pubmed_authors>Melis V</pubmed_authors><pubmed_authors>Platt B</pubmed_authors><pubmed_authors>Riedel G</pubmed_authors><pubmed_authors>Mondesir M</pubmed_authors><pubmed_authors>Harrington CR</pubmed_authors></additional><is_claimable>false</is_claimable><name>Effect of the Icelandic Mutation APP&lt;sup>A673T&lt;/sup> in the Murine APP Gene on Phenotype of Line 66 Tau Mice.</name><description>The Icelandic mutation in the amyloid precursor protein (APP), APP&lt;sup>A673T&lt;/sup>, has been identified in Icelandic and Scandinavian populations and is associated with a significantly lower risk of developing Alzheimer's disease (AD). The introduction of the human APP&lt;sup>A673T&lt;/sup> form led to a reduction in amyloid β-protein (Aβ) production and tau pathology, but the effect of mouse APP&lt;sup>A673T&lt;/sup> on tau and Aβ pathology is not well studied. We have crossed line 66 (L66) tau transgenic mice that overexpress the P301S aggregation-prone form of tau with C57Bl6/J mice expressing a single-point mutation edited into the murine &lt;i>APP&lt;/i> gene via CRISPR-Cas gene editing, known as mAPP&lt;sup>A673T&lt;/sup>. We have performed ELISA, histopathological, and behavioural analyses of heterozygous </description><dates><release>2025-01-01T00:00:00Z</release><publication>2025 Dec</publication><modification>2026-06-11T03:16:43.019Z</modification><creation>2026-06-11T03:12:17.221Z</creation></dates><accession>S-EPMC12838599</accession><cross_references><pubmed>41594570</pubmed><doi>10.3390/biom16010028</doi></cross_references></HashMap>