Modification: APP: Transgenic
Disease Relevance: Alzheimer's Disease
Strain Name: B6.Cg-Tg(PDGFB-APP)5Lms/J
Genetic Background: (C57BL/6 x DBA/2)F2
Availability: The Jackson Lab: Stock# 004662; Cryopreserved
These transgenic mice express wild-type human APP under the control of the human PDGF-β promoter. They were generated as control mice for the J20 model. They express human APP in neurons throughout the brain, with maximal levels in the neocortex and hippocampus. No plaques were observed out to 24 months, but synaptophysin immunoreactivity decreases with age (Mucke et al., 2000).
APP-WT driven by the human PDGF-β promoter; an APP transgene with the Indiana mutation was converted to wild-type by PCR primer modification.
When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.
- Neuronal Loss
By 2-4 months of age, there is a decrease in synaptophysin-immunoreactive presynaptic terminals compared to nonTg controls. Synaptophysin immunoreactivity decreases further with age.
Research Models Citations
- Mucke L, Masliah E, Yu GQ, Mallory M, Rockenstein EM, Tatsuno G, Hu K, Kholodenko D, Johnson-Wood K, McConlogue L. High-level neuronal expression of abeta 1-42 in wild-type human amyloid protein precursor transgenic mice: synaptotoxicity without plaque formation. J Neurosci. 2000 Jun 1;20(11):4050-8. PubMed.
No Available Further Reading