Mouse models are likely to remain the workhorses for the in vivo modeling of AD pathogenesis. The advantages of speed, economy, and reasonably compelling lesion development are likely to improve as new models are developed and refined. There remains a disconnect between current models and the profound neurodegeneration that is prominent in AD. Filling this gap is the most important mechanistic need. Present models are sufficient for testing many of the current therapeutic avenues being explored. However, if time is an essential and immutable element in the ultimate manifestation of AD, and many years are required for the full phenotype to emerge, then the expression of AD-related transgenes in longer-lived species, such as nonhuman primates, could provide an important bridge between mouse models and the human disease. To this end, the expression of disease-related transgenes in adult animals via viral vectors, which has produced a remarkably Parkinsonian phenotype in nonhuman primates (Kirik et al., 2003), has potential for more faithfully recapitulating the full neuropathological phenotype of AD. At the other end of the taxonomic spectrum, advances in modeling AD pathology in lower organisms such as fruit flies and worms will be a boon to testing mechanistic hypotheses at the cellular and molecular levels.
Since AD is a uniquely human disorder, the thoughtful integration of experimental information from cellular, nonmammalian and mammalian models will be needed to achieve a comprehensive view of the natural history of the Alzheimer's disease process.
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