Research Models
PDGF-APP(WT) (line I5)
Species: Mouse
Genes: APP
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).
Modification Details
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.
Phenotype Characterization
When visualized, these models will distributed over a 18 month timeline demarcated at the following intervals: 1mo, 3mo, 6mo, 9mo, 12mo, 15mo, 18mo+.
Absent
- Tangles
- Neuronal Loss
No Data
Tangles
Not observed.
Neuronal Loss
Not observed.
Synaptic 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.
Last Updated: 25 Nov 2019
References
Research Models Citations
Paper 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.
External Citations
Further Reading
No Available Further Reading
COMMENTS / QUESTIONS
No Available Comments
Make a comment or submit a question
To make a comment you must login or register.