Article
A Trem2R47H mouse model without cryptic splicing drives age- and disease-dependent tissue damage and synaptic loss in response to plaques.
Molecular neurodegeneration - 17 Feb 2023
Tran Kristine M, Kawauchi Shimako, Kramár Enikö A, Rezaie Narges, Liang Heidi Yahan, Sakr Jasmine S, Gomez-Arboledas Angela, Arreola Miguel A, Cunha Celia da, Phan Jimmy, Wang Shuling, Collins Sherilyn, Walker Amber, Shi Kai-Xuan, Neumann Jonathan, Filimban Ghassan, Shi Zechuan, Milinkeviciute Giedre, Javonillo Dominic I, Tran Katelynn, Gantuz Magdalena, Forner Stefania, Swarup Vivek, Tenner Andrea J, LaFerla Frank M, Wood Marcelo A, Mortazavi Ali, MacGregor Grant R, Green Kim N
Abstract excerpt
BACKGROUND: The TREM2 R47H variant is one of the strongest genetic risk factors for late-onset Alzheimer's Disease (AD). Unfortunately, many current Trem2 R47H mouse models are associated with cryptic mRNA splicing of the mutant allele that produces a confounding reduction in protein product. To overcome this issue, we developed the Trem2R47H NSS (Normal Splice Site) mouse model in which the Trem2 allele is...
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