Immunodeficient Mice

Disease phenotypes can vary substantially among mouse strains with different genetic backgrounds. These variations may manifest as entirely distinct phenotypes, differences in phenotypic penetrance, or variable expressivity of the phenotype. For example: C57BL/6 and BALB/c mice differ in their Th1 and Th2 immune responses. In C57BL/6 mice, Th1 immune responses and interferon-gamma (IFN-γ) production predominate, whereas BALB/c mice are highly prone to mounting Th2 immune responses, a divergence commonly observed in infectious diseases and allergic reactions. The immunological differences between BALB/c and C57BL/6 mice directly influence the pathogenesis and disease onset of certain autoimmune models. While both C57BL/6 and BALB/c share the advantage of genetic homogeneity inherent to inbred strains, applying them to immunological research requires careful consideration of their numerous physiological and immunological differences. The selection of the background strain should be guided strictly by the specific research objectives and experimental design.

Each AD mouse model developed by GemPharmatech is tailored to address distinct pathological mechanism research and drug development requirements. FAD4T model: Best suited for drug development targeting mild-to-moderate AD. This model exhibits amyloid-beta (Aβ) plaque deposition starting at 2 months of age, which progressively worsens with disease advancement, followed by the onset of cognitive impairment at 8 months of age. FAD2T model: Ideal for vaccine candidate evaluation or drug development targeting mild AD. Aβ plaque deposition begins at 4 months of age, offering an efficacy evaluation window of approximately 3 months for vaccines (prior to extensive plaque pathology). Although cognitive impairment also manifests at 8 months of age, the overall plaque burden is significantly lower than that of the FAD4T model, making it highly suitable for investigating early-stage or mild pathological progression. FAD3T model: Designed for drug development targeting moderate-to-severe AD. In addition to Aβ plaque deposition, this model incorporates tau hyperphosphorylation pathology. Alterations in clinically relevant biomarkers—such as p-Tau181, p-Tau217, Aβ, and neurofilament light chain (NfL)—are detectable as early as 1 month of age. The onset of cognitive impairment exhibits sexual dimorphism (3 months of age in females; 4 months of age in males), recapitulating the gender-related differences observed clinically. This provides a highly comprehensive model for evaluating therapeutics and diagnostic assays for advanced-stage AD pathology.