References
Query Results -- Details
MGI Accession ID: MGI:73228
J Number: J:25512
Other Accession IDs:
Title: beta-Amyloid precursor protein-deficient mice show reactive gliosis and decreased locomotor activity.
Authors: Zheng H; Jiang M; Trumbauer ME; Sirinathsinghji DJ; Hopkins R; Smith DW; Heavens RP; Dawson GR; Boyce S; Conner MW; Stevens KA; Slunt HH; Sisodia SS; Chen HY; Van der Ploeg LHT
Journal: Cell
Volume: 81
Issue: 4
Date: 1995 May 19
Year: 1995
Pages: 525-31
Review Status: Peer Reviewed
Abstract:
In several pedigrees of early onset familial Alzheimer's disease (FAD), point mutations in the beta-amyloid precursor protein (APP) gene are genetically linked to the disease. This finding implicates APP in the pathogenesis of Alzheimer's disease in these individuals. To understand the in vivo function of APP and its processing, we have generated an APP-null mutation in mice. Homozygous APP-deficient mice were viable and fertile. However, the mutant animals weighed 15%-20% less than age-matched wild-type controls. Neurological evaluation showed that the APP-deficient mice exhibited a decreased locomotor activity and forelimb grip strength, indicating a compromised neuronal or muscular function. In addition, four out of six homozygous mice showed reactive gliosis at 14 weeks of age, suggesting an impaired neuronal function as a result of the APP-null mutation.
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