The human TREM gene cluster (TREML1 to NCR2) is associated with Alzheimer's Disease pathogenesis and microglial function. Specifically, Trem2 (triggering receptor expressed on myeloid cells 2) encodes a protein that is a part of a receptor signaling complex with TYRO protein tyrosine kinase binding protein that activates macrophages and dendritic cells during immune responses. The humanized transchromosomal rs9357347-C TREM-GR (gene replacement) mice are a knock-in/knock-out model in which the mouse genomic region (Chr17:48,404,707-48,693,648) between Treml1 (triggering receptor expressed on myeloid cells like 1) to Trem1 (triggering receptor expressed on myeloid cells 1) is replaced by the human TREM gene cluster containing TREML1, TREM2, TREML2, TREML4, TREM1, and NCR2 (including promoter, regulatory and intergenic regions; Chr6:41,099,491-41,379,205). In these mice, the human segment includes a rs9357347-C non-coding protective variant. This SNP is a regulatory variant that modulates both beta-amyloid pathology and neuronal degeneration and is associated with a decreased risk of Alzheimer's disease. Homozygous mice are viable and fertile with no obvious anatomical or behavior issues. Of note, a set of TREM2-GR strains are distributed as B6J.B6N-Tc(HSA6)1Mdk/J; WT-TREM2-GR (Stock No. <a href="https://www.jax.org/strain/039172">039172</a>), B6J.B6N-Tc(HSA6_TREM2*R47H)1Mdk/J; R47H-TREM2-GR (Stock No. <a href="https://www.jax.org/strain/039173">039173</a>), and B6J.B6N-Tc(HSA6*rs9357347-C)1Mdk/J; rs9357347-C-TREM2-GR (this strain, Stock No. 039174).

Humanized transchromosomal rs9357347-C TREM2-GR (gene replacement) mice are a knock-in/knock-out model in which a 289 kb region of mouse chromosome 17 including Trem2 (triggering receptor expressed on myeloid cells 2) is exchanged for 280 kb of the human TREML1 to NCR2 (including TREM2) genomic region on chromosome 6 (HSA6). In these mice, a rs9357347-C non-coding protective variant is present. The rs9357347 SNP is located 6.9 kb downstream from TREML2 and 19.6 kb upstream from TREM2. These mice may serve as base models into which additional alterations can be introduced to explore more fully the role of the TREM gene cluster in Alzheimer's disease (AD).

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