APP knockout mouse
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Introduction
APP knockout mice do not exhibit early mortality, but display some abnormalities.
The phenotype is characterized by:[1]
- reduced weight
- decreased neuromuscular performance
- reactive gliosis in the hippocampus & cortex (later in adult life)
- reduced synaptic plasticity
- loss of synaptic immunoreactivity for:
- defects in the corpus callosum
It is suggested that APP is one of a family of proteins (the APLP family of proteins) with overlapping function, thus the apparent non essentiality of a single member of the family.[2]
More general terms
Additional terms
References
- ↑ 1.0 1.1 Kamal A, Almenar-Queralt A, LeBlanc JF, Roberts EA, Goldstein LS. Kinesin-mediated axonal transport of a membrane compartment containing beta-secretase and presenilin-1 requires APP. Nature. 2001 Dec 6;414(6864):643-8. PMID: https://www.ncbi.nlm.nih.gov/pubmed/11740561
- ↑ 2.0 2.1 Selkoe DJ. Alzheimer's disease: genes, proteins, and therapy. Physiol Rev. 2001 Apr;81(2):741-66. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/11274343