Lack of beta-amyloidosis in transgenic mice expressing low levels of familial Alzheimer's disease missense mutations.

Malherbe, P; Richards, J G; Martin, J R; Bluethmann, H; Maggio, J; Huber, G

Malherbe, P; Richards, J G; Martin, J R; Bluethmann, H; Maggio, J; Huber, G.

Affiliation

Malherbe P; Pharma Division, F. Hoffmann-La Roche Ltd., Basel, Switzerland.

Neurobiol Aging ; 17(2): 205-14, 1996.

Article in En | MEDLINE | ID: mdl-8744401

Subject(s)

Alzheimer Disease/genetics; Amyloidosis/genetics; Amyloidosis/pathology; Point Mutation/physiology; Alzheimer Disease/metabolism; Alzheimer Disease/pathology; Amyloid beta-Peptides/biosynthesis; Amyloid beta-Peptides/genetics; Amyloidosis/psychology; Animals; Base Sequence; Behavior, Animal/physiology; Blotting, Southern; Blotting, Western; Humans; Immunohistochemistry; In Situ Hybridization; Mice; Mice, Inbred C57BL; Mice, Transgenic; Molecular Sequence Data; Phosphopyruvate Hydratase/genetics; Point Mutation/genetics; Polymerase Chain Reaction; RNA, Messenger/biosynthesis; Transgenes/genetics

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Collection: 01-internacional Database: MEDLINE Main subject: Point Mutation / Alzheimer Disease / Amyloidosis Limits: Animals / Humans Language: En Journal: Neurobiol Aging Year: 1996 Type: Article Affiliation country: Switzerland

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