Mutations: APP KM670/671NL (Swedish)
Modification: APP: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: N/A
Genetic Background: Origin: C57BL/6 x DBA/2
Availability: Available through Yong K Kim.
Increased Aβ42 in the cortex and hippocampus of 12 month-old mice, but no plaques. Increased tau phosphorylation and TUNEL-stained nuclei relative to control mice (Hwang et al., 2004).
In water maze tests, 12 month-old mice had longer escape latencies than age-matched control mice (Hwang et al., 2004).
Metallothionein expression was increased in brain astrocytes and was thought to attenuate Aβ-induced neurotoxicity (Kim et al., 2012). Cox-2 and caspase-3 were also elevated compared to age-matched control mice (Hwang et al., 2004).
These transgenic mice express human APP (isoform 695) bearing the Swedish mutation under the control of the neuron specific enolase (NSE) promoter.
- Hwang DY, Cho JS, Lee SH, Chae KR, Lim HJ, Min SH, Seo SJ, Song YS, Song CW, Paik SG, Sheen YY, Kim YK. Aberrant expressions of pathogenic phenotype in Alzheimer's diseased transgenic mice carrying NSE-controlled APPsw. Exp Neurol. 2004 Mar;186(1):20-32. PubMed.
- Kim JH, Nam YP, Jeon SM, Han HS, Suk K. Amyloid neurotoxicity is attenuated by metallothionein: dual mechanisms at work. J Neurochem. 2012 Jun;121(5):751-62. PubMed.
No Available Further Reading