| 摘要 |
In accordance with the present invention, it is demonstrated that selected mutations such as an Asp -> Ala (D664A) mutation in APP (which prevents cleavage at the caspase cleavage site) prevent both hippocampal synaptic los s and dentate gyral atrophy, even though such mutations do not interfere with the production of A~ or the formation of amyloid plaques in a transgenic mod el of Alzheimer's disease. Accordingly, in view of this finding, methods have been developed for the identification of agents which block cleavage at Asp6 64 of APP, including transgenic animals which are useful for such purpose, as well as methods for the use thereof for the treatment of neurodegenerative diseases.
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