CVN mice (APP with Swedish, Dutch and Iowa mutations crossed with NOS2 knockout) provide a new tool for Alzheimer’s disease (AD) studies. The mice exhibit behavioral deficits as well as biochemical hallmarks of AD during aging. There is a marked inflammatory component in the mice compared to the Tg2576 line, and amyloid plaques and insoluble amyloid are detectable in mice at 9 months of age.
To learn more about this model and how it compares to other animal models of Alzheimer’s disease, watch our webinar titled “CVN Mouse: A More Translatable Alzheimer's Efficacy Model” (available only in the Source℠). If you are not a member of the Source℠, our online scientific and educational information center, please click here to register
Example Study Paradigms of CVN Mouse Model
Click here to see a diagram outlining an example 36-week study paradigm using CVN mouse model.
Click here to see a diagram outlining an example 16-week study paradigm using CVN mouse model.
Behavioral Deficits in 9-Month-Old CVN Mice
The APPSwDI/NOS2-/- mice had decreased latency to correct hole on test days 3-5 compared to WT mice in Barnes maze.
Radial Arm Water Maze
The APPSwDI/NOS2-/- mice had decreased latency on radial arm water maze on test days 1and 2 compared to WT mice.
CVN mice show amyloid plaques in the hippocampus, cortex and thalamus. In addition, the amount of insoluble Aβ1-40 and 1-42 is increased in these animals at 9-12 months.
CVN mice show increased microgliosis compared to wild-type (wt) mice during aging. Iba-1 antibody was used to detect microglial cells.
Synaptophysin qPRC for Synaptic Marker
Cortical synaptophysin mRNA level is significantly decreased in CVN mice at 9 months of age.
For more information about our Alzheimer’s disease research studies with the CVN mouse, please contact us at 1.877.CRIVER.1 or firstname.lastname@example.org.