A large number of genetic disease model mice have been produced by genetic engineering.
It has been reported that neurons from AS model mice have abnormal spine morphology13 and decreases in the frequency of both spontaneous excitatory and inhibitory postsynaptic currents9.
However, in our present study, another mammalian model, mice have been used.
Studies using HD model mice have identified many genes whose expression is altered by mutant huntingtin (4– 7).
Muenke model mice have craniofacial phenotypes that vary in penetrance and expressivity depending on genetic background, but do not include obvious middle ear anomalies.
In the MINO model, mice have been engineered to have neoplastic outgrowths from mammary ducts [ 7, 8] while in the MIND model, human DCIS cell lines are transplanted intraductally to mimic the structure of DCIS found in humans [ 9, 10].
Brains from IAE model mice had significantly higher expression of type I interferons and inflammatory cytokines.
Whereas the autism model mice had too few gastrointestinal neurons and a slow-moving gut, the SSRI and SERTKO pups had too many neurons and a fast-moving gut.
Accordingly, IFN-α production in IBD model mice has been noted in both CD11b+ and CD11c+ dendritic cells in colonic lamina propria [ 60].
Thus, rodent models, and particularly mice, have become the most widely used models of human disease.
