login

β-amyloid precursor protein-deficient mice show reactive gliosis and decreased locomotor activity

CellPublished 1 May 1995Open access
Hui Zheng, Minghao Jiang, Myrna E. Trumbauer, D.J.S. Sirinathsinghji, Ruth Hopkins, David W. Smith
Citations702
SJR quartileQ1
SJR score22.61
SNIP7.62
View PDF

TL;DR

To understand the in vivo function of APP and its processing, an APP-null mutation is generated in mice and it is shown that the APP-deficient mice exhibited a decreased locomotor activity and forelimb grip strength, indicating a compromised neuronal or muscular function.

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.

Keywords

MedicineBiochemistry, Genetics and Molecular Biology