AD may in many ways be regarded as the ideal disease for modeling in transgenic animals. First, it has a well-recognized pathology consisting of senile plaques and NFTs. The major constituents of these lesions are well defined, being the β-amyloid (Aβ) peptide in the case of plaques and hyperphosphorylated forms of tau in NFTs. AD also has other well-recognized pathological features, including neuronal and synaptic loss, dystrophic neurites, reactive astrocytes, and activated microglia. There is, in addition, a well-defined behavioral phenotype that can be modeled in the mouse.
