Although human GWAS associations have been documented in agnostic experiments, the mouse models are typically constructed to test a specific hypothesis, which is usually based on various types of biological evidence.
Subcutaneous xenograft mouse models are typically the standard for cancer drug screening in the pharmaceutical industry [ 9], but the use of orthotopic xenotransplantation models should be favored since tissue specific stromal cell interactions play a crucial role in the biology of cancer progression and metastasis.
Mouse colitis models typically show features like crypt elongation due to increased cell proliferation, infiltration of immune cells in lamina propria, thickening of muscularis propria and weight loss, all criteria used for scoring colitis 33, 34.
In the NOD mouse model, insulitis typically begins around 3 4 weeks of age, and diabetes occurs in 60 80% of female mice between 12 18 weeks of age depending on the housing conditions.
Mouse models of cGvHD typically involve three main pathological mechanisms: autoantibody production, pro-fibrotic pathways and defective thymic function.
These dynamics could easily be overlooked in mutant mouse models that are typically assessed only by dendritic spine density in adults.
Nowadays, these mouse models of AD are typically transgenic (tg) mice carrying mutations in the APP, PS1 or PS2 gene.
In chemically induced plasmacytoma mouse models, plasmacytoma cells are typically located at the site of injection and infrequently metastasize to BM and other organs.
Mouse models mimicking AD-typical pathology, such as deficits in synaptic transmission [ 24], changes in behavior, differential glutamate responses, and deficits in long-term potentiation are typically based on the overexpression of full-length amyloid precursor protein (APP) [ 39].
Given the rapid growth of the B16F10 model and ethical limitations of animal studies, studies using this pre-clinical mouse model is limited typically to a single round of therapy.
