Abstract: In its various embodiments, the invention provides myelin basic proteins and fragments of that interfere with the fibrillization of peptides implicated in the amyloidoses, especially the amyloid-b eta peptide associated with Alzheimer's disease (“AD”) and cerebral amyloid angiopathy (“CAA”). Some embodiments provide methods of identifying additional interfering fragments. Others provide methods of identifying substances that modulate the interference. Further embodiments provide methods of preventing amyloidoses, especially AD and CAA by administering myelin basic proteins or fragments thereof.

Abstract: In its various embodiments, the invention provides myelin basic proteins and fragments of that interfere with the fibrillization of peptides implicated in the amyloidoses, especially the amyloid-b eta peptide associated with Alzheimer's disease (“AD”) and cerebral amyloid angiopathy (“CAA”). Some embodiments provide methods of identifying additional interfering fragments. Others provide methods of identifying substances that modulate the interference. Further embodiments provide methods of preventing amyloidoses, especially AD and CAA by administering myelin basic proteins or fragments thereof.

Abstract: In its various embodiments, the invention provides myelin basic proteins and fragments of that interfere with the fibril lization of peptides implicated in the amyloidoses, especially the amyloid-beta peptide associated with Alzheimer's disease (“AD”) and cerebral amyloid angiopathy (“CAA”). Some embodiments provide methods of identifying additional interfering fragments. Others provide methods of identifying substances that modulate the interference. Further embodiments provide methods of preventing amyloidoses, especially AD and CAA by administering myelin basic proteins or fragments thereof.

Abstract: In its various embodiments, the invention provides myelin basic proteins and fragments of that interfere with the fibril lization of peptides implicated in the amyloidoses, especially the amyloid-beta peptide associated with Alzheimer's disease (“AD”) and cerebral amyloid angiopathy (“CAA”). Some embodiments provide methods of identifying additional interfering fragments. Others provide methods of identifying substances that modulate the interference. Further embodiments provide methods of preventing amyloidoses, especially AD and CAA by administering myelin basic proteins or fragments thereof.

Abstract: Monoclonal antibody and the hybridoma producing the antibody are disclosed. The antibody is produced against an epitope on native secreted forms of .beta.APP. A characteristic of the antibody is that the antibody specifically binds to at least one protein in culture medium in which neuroblastoma cells have been grown. This protein co-migrates in non-reducing polyacrylamide gel electrophoresis with PN-2 isolated from human fibroblast cultures. Other characteristics of the antibody are that the antibody specifically binds to PN-2 and to the secreted form of .beta.APP lacking the Kunitz-type inhibitor domain, the antibody selectively binds to neuritic plaques, and the antibody is sufficiently sensitive to detect secreted forms of .beta.APP in CSF, down to a total concentration of the secreted forms of .beta.APP of 3.75 .mu.g/ml or lower.

Abstract: A method of diagnosing a disease with cerebrovascular deposition of amyloid, including Alzheimer's disease, hereditary cerebral hemorrhage with amyloidosis-Dutch type and other amyloidoses, in a mammal is disclosed in which a sample of cerebrospinal fluid is obtained, the level of immunoreactivity toward a monoclonal antibody raised against native PN-2/.beta.APP or other amyloid precursor protein in the sample is measured, and this measured level is compared to the level of immunoreactivity toward this antibody in a sample fromNOTICE OF GOVERNMENT SUPPORTThis invention was made with Government support under Grant No. GM-31609 awarded by the National Institutes of Health. The Government has certain rights in this invention. American Cancer Society Grants CD 390 and BC 602/BE 22A provided further support for the development of this invention.

Abstract: Immunopurification of Protease Nexin-2 and .beta. amyloid precursor protein is disclosed. Methods of detecting Protease Nexin-2 and the use of these methods in the diagnosis of Alzheimer's disease and other conditions are also disclosed. Additionally, pharmaceutical preparations including Protease Nexin-2 or modified forms thereof are disclosed. Medical uses for the pharmaceutical preparations are also disclosed.

Abstract: Monoclonal antibodies having a specificity for protease nexin-1 are described. Preferably an antibody has specificity to the reactive protease-binding site. The antibody is used in the affinity purification of PN-1 to produce large quantities of substantially pure PN-1, free of other biologically active molecules. Over a 2000-fold purification of a crude preparation of PN-1 may be obtained. The affinity-purified PN-1 is suitable for use in pharmacological preparations used in the treatment of neurological disease associated with serine protease-mediated inhibition of regenerative processes.