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Development of mouse models is critical for expanding our understanding of the causes of schizophrenia.
The knowledge generated in mouse models, even in humanized mouse models, is not directly applicable to humans.
This phenotypic difference between the two mouse models is because of the differences in the ganglioside degradation pathway between mice and humans.
The global obesity epidemic has heightened the need for an improved understanding of how body weight is controlled, and research using mouse models is critical to this effort.
One of the most commonly used tau mouse models is the tet-off Tg tauP301L 4510 model that expresses P301L human tau driven by the calcium calmodulin kinase IIα (CaMKIIα) promoter system.
An important difference in the two mouse models is the amount of beta-amyloid and plaque load.
Moving forward and testing the hypothesis of haploinsufficiency as a disease mechanism is difficult, and using mouse models is problematic.
An important consideration in the characterization of AD transgenic mouse models is the qualitative and quantitative evaluation of amyloid load in the brain.
Altogether, these facts stress the need to investigate systematically whether the data generated in mouse models is relevant in a clinical setting.
One major difference between our study and previous studies of DENV infection in humanized mouse models is our demonstration of IFN-γ production by human T cells in response to DENV-2 antigen and virus-specific peptides.
The role for SpeB as virulence factor in mouse models is not uncontroversial and there have been reports using SpeB deletion mutants indicating that SpeB is not a virulence factor [9], [10].
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