Posted 27 June 2010
Transgene: Human APP695 containing the Swe (K670N + M671L) and Arc mutations (E693G)
was generated by site directed mutagenesis of pGEM-9zf(-)-huAPP695. The cDNA was
inserted into pMoPrP-Xho, and the construct was sequenced. After removal of the
vector sequence, the linear construct was injected into pronuclei of fertilized
zygotes of B6D2F1 mice.
Mouse Strain: Origin: B6D2 F1
At 6 months intracellular punctate deposits of Aβ were abundant in cortex and
hippocampus with no apparent β-amyloid plaque load. Between 9 and 15 months
of age, β-amyloid plaques became a prominent feature in our arcAβ mice.
Severe CAA was also present at this age; with dense Aβ aggregates decorating
blood vessels walls and spreading from there into the parenchyma.
The arcAβ mice were cognitively impaired from the age of 6 months on in MWM
and Y-maze as well as in active avoidance behavior.
Roger M. Nitsch
Division of Psychiatry Research, University of Zurich
August Forel-Str. 1
8008 Zurich, Switzerland
Phone: +41 44 634 8870
Fax: +41 44 634 8876
Knobloch M, Konietzko U, Krebs DC, Nitsch RM. Intracellular Abeta and cognitive
deficits precede beta-amyloid deposition in transgenic arcAbeta mice. Neurobiol
Aging. 2007 Sep;28(9):1297-306.
Vodopivec I, Galichet A, Knobloch M, Bierhaus A, Heizmann CW, Nitsch RM. RAGE does
not affect amyloid pathology in transgenic ArcAbeta mice. Neurodegener Dis. 2009;6(5-6):270-80.