The missing link in current animal models for AD is the lack of the profound neurodegeneration of AD. In the context of animal models of other diseases, as mentioned earlier, this is common. Often, different species model particular aspects of the human disease, but not others, so multiple models are used for each disease. A compounding factor for AD is that it is a disease of aging, and extreme age at that. Mice may simply not live long enough to produce the decrements in neuronal structure and function. Longer lived models, on the order of the human lifespan, that recapitulated the disease would be of academic and mechanistic interest, but not practical for testing therapeutic interventions. It is possible that critical pathways that couple insults such as Ap aggregation to toxicity and neurodegeneration are deficient in mice, or that there is a compensating pathway. Processes that magnify the toxic effects of Ap, such as inflammation, may be attenuated in mice. Compounding this could be an intrinsic difference in the plaque structure (Klunk et al., 2004) or composition compared to the AD brain.
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