{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Anschuetz A"],"funding":["TauRx Therapeutics Ltd Singapore"],"pagination":["28"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC12838599"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["16(1)"],"pubmed_abstract":["The Icelandic mutation in the amyloid precursor protein (APP), APP<sup>A673T</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<sup>A673T</sup> form led to a reduction in amyloid β-protein (Aβ) production and tau pathology, but the effect of mouse APP<sup>A673T</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 <i>APP</i> gene via CRISPR-Cas gene editing, known as mAPP<sup>A673T</sup>. We have performed ELISA, histopathological, and behavioural analyses of heterozygous "],"journal":["Biomolecules"],"pubmed_title":["Effect of the Icelandic Mutation APP<sup>A673T</sup> in the Murine APP Gene on Phenotype of Line 66 Tau Mice."],"pmcid":["PMC12838599"],"funding_grant_id":["PAR1577 and PAR2074"],"pubmed_authors":["Anschuetz A","Robinson L","Schwab K","Melis V","Platt B","Riedel G","Mondesir M","Harrington CR"],"additional_accession":[]},"is_claimable":false,"name":"Effect of the Icelandic Mutation APP<sup>A673T</sup> in the Murine APP Gene on Phenotype of Line 66 Tau Mice.","description":"The Icelandic mutation in the amyloid precursor protein (APP), APP<sup>A673T</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<sup>A673T</sup> form led to a reduction in amyloid β-protein (Aβ) production and tau pathology, but the effect of mouse APP<sup>A673T</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 <i>APP</i> gene via CRISPR-Cas gene editing, known as mAPP<sup>A673T</sup>. We have performed ELISA, histopathological, and behavioural analyses of heterozygous ","dates":{"release":"2025-01-01T00:00:00Z","publication":"2025 Dec","modification":"2026-06-11T03:16:43.019Z","creation":"2026-06-11T03:12:17.221Z"},"accession":"S-EPMC12838599","cross_references":{"pubmed":["41594570"],"doi":["10.3390/biom16010028"]}}