Abstract
AβPP transgenic mice replicate some aspects of Alzheimers disease pathology. Despite some similarities, significant biochemical and physical differences exist between the amyloid deposits characteristic of transgenic animals and AD patients. These differences may account for the fact that the promising results obtained by amyloid vaccination of AβPP transgenic mice were not replicated in humans. Aβ is an evolutionarily-conserved molecule of unknown function. Future therapeutic strategies directed toward interfering with amyloid production should be implemented with caution.
Keywords: beta amyloid, alzheimer disease, transgenic mice, therapeutic intervention, amyloid precursor protein, senile plaque, immunization, post-translational modification
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