Caine W. Wong
University of California, San Diego
7 Papers
92 Citations
Caine W. Wong is an academic researcher from University of California, San Diego. The author has contributed to research in topics: BACE1-AS & P3 peptide. The author has an hindex of 6, co-authored 7 publications.
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Papers
Alzheimer's disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid protein
George G. Glenner,Caine W. Wong +1 more
TL;DR: A purified protein derived from the twisted beta-pleated sheet fibrils in cerebrovascular amyloidosis associated with Alzheimer's disease has been isolated and Amino acid sequence analysis and a computer search reveals this protein to have no homology with any protein sequenced thus far.
5.2K
Alzheimer's disease and Down's syndrome: sharing of a unique cerebrovascular amyloid fibril protein.
George G. Glenner,Caine W. Wong +1 more
TL;DR: The cerebrovascular amyloid protein from a case of adult Down's syndrome was isolated and purified and Amino acid sequence analysis showed it to be homologous to that of the beta protein of Alzheimer's disease.
1.8K
Neuritic plaques and cerebrovascular amyloid in Alzheimer disease are antigenically related
TL;DR: It is suggested that the amyloid in neuritic plaques shares antigenic determinants with beta protein of cerebral vessels and this possibility suggests a model for the pathogenesis of Alzheimer disease involving beta protein.
488
Immunohistochemical evidence for the derivation of a peptide ligand from the amyloid beta-protein precursor of Alzheimer disease
TL;DR: Results from immunohistochemical studies suggest that the beta-protein precursor may be processed to release an active peptide ligand rather than acting as a membrane receptor in Alzheimer disease.
73
Amyloid β-protein gene duplication is not common in Alzheimer's disease: Analysis by polymorphic restriction fragments
TL;DR: It is concluded that BP gene duplication is rare, if any, in (Japanese) sporadic AD patients, indicating that the duplication of the BP gene itself is not the common underlying genetic defect in AD.
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