Abstract: Disclosed are microcapsules that include an inhibitor of the mammalian target of rapamycin (mTOR) within the microcapsules, and pharmaceutical compositions and kits that include the microcapsules. Also disclosed are methods for treating or preventing an age-related disease, condition, or disorder in a subject that involve administering to a subject a pharmaceutically effective amount of microcapsules that includes an inhibitor of mTOR within the microcapsules.

Abstract: Disclosed are microcapsules that include an inhibitor of the mammalian target of rapamycin (mTOR) within the microcapsules, and pharmaceutical compositions and kits that include the microcapsules. Also disclosed are methods for treating or preventing an age-related disease, condition, or disorder in a subject that involve administering to a subject a pharmaceutically effective amount of microcapsules that includes an inhibitor of mTOR within the microcapsules.

Abstract: Disclosed are microcapsules that include an inhibitor of the mammalian target of rapamycin (mTOR) within the microcapsules, and pharmaceutical compositions and kits that include the microcapsules. Also disclosed are methods for treating or preventing an age-related disease, condition, or disorder in a subject that involve administering to a subject a pharmaceutically effective amount of microcapsules that includes an inhibitor of mTOR within the microcapsules.

Abstract: Disclosed are methods and compositions for preventing cerebrovascular function dysfunction in a patient who has been identified as an ApoE4 carrier. The disclosed methods and compositions include rapamycin, a rapamycin analog, or another such inhibitor of the target of rapamycin (TOR).

Abstract: Disclosed are methods and compositions for the treatment or prevention of vascular cognitive impairment. The disclosed methods and compositions include rapamycin, a rapamycin analog, or another such inhibitor of the target of rapamycin (TOR).

Abstract: The invention provides methods and compositions for reducing or inhibiting net beta-amyloid peptide production and/or amyloid plaque formation. The methods and compositions involve administering a netrin-1 polypeptide or netrin-1 therapeutic to a subject in need thereof.

Abstract: Disclosed are microcapsules that include an inhibitor of the mammalian target of rapamycin (mTOR) within the microcapsules, and pharmaceutical compositions and kits that include the microcapsules. Also disclosed are methods for treating or preventing an age-related disease, condition, or disorder in a subject that involve administering to a subject a pharmaceutically effective amount of microcapsules that includes an inhibitor of mTOR within the microcapsules.

Abstract: The invention provides a method for reducing or inhibiting net beta-amyloid peptide production and amyloid plaque formation associated with Alzheimer's Disease by administering to a subject an amount of a netrin-1 polypeptide, wherein the netrin-1 polypeptide comprises an amino acid sequence that a) binds to a naturally occurring APP protein and b) inhibits A? peptide production. A netrin-1 polypeptide has an amino acid sequence sufficient for specific binding of the netrin-1 polypeptide to the APP protein. A netrin-1 polypeptide can mimic netrin-1-mediated signal transduction by altering the localization, protein-protein binding and/or enzymatic activity of an intracellular protein involved in an APP signal pathway.

Abstract: 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 loss 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 model of Alzheimer's disease. Accordingly, in view of this finding, methods have been developed for the identification of agents which block cleavage at Asp664 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.

Abstract: 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 loss 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 model of Alzheimer's disease. Accordingly, in view of this finding, methods have been developed for the identification of agents which block cleavage at Asp664 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.