Journal
ACTA NEUROPATHOLOGICA COMMUNICATIONS
Volume 3, Issue -, Pages -Publisher
BMC
DOI: 10.1186/s40478-015-0252-9
Keywords
-
Categories
Funding
- National Institutes of Neurological Disease and Stroke [R01 NS 047225]
- SantaFe Healthcare Alzheimer's Disease Research Center
Ask authors/readers for more resources
Introduction: Transgenic overexpression of amyloid precursor protein (APP) genes that are either entirely human in sequence or have humanized A beta sequences can produce Alzheimer-type amyloidosis in mice, provided the transgenes also encode mutations linked to familial Alzheimer's Disease (FAD). Although transgenic mice have been produced that overexpress wild-type mouse APP, no mice have been generated that express mouse APP with FAD mutations. Here we describe two different versions of such mice that produce amyloid deposits consisting of entirely of mouse A beta peptides. One line of mice co-expresses mouse APP-Swedish (moAPPswe) with a human presenilin exon-9 deleted variant (PS1dE9) and another line expresses mouse APP-Swedish/Indiana (APPsi) using tetracycline-regulated vectors (tet.moAPPsi). Results: Both lines of mice that produce mouse A beta develop amyloid deposits, with the moAPPswe/PS1dE9 micedeveloping extracellular compact, cored, neuritic deposits that primarily localize to white matter tracts andmeningial layers, whereas the tet. moAPPsi mice developed extracellular diffuse cortical/hippocampal deposits distributed throughout the parenchyma. Conclusions: These findings demonstrate that murine A beta peptides have the capacity to produce amyloid deposits that are morphologically similar to deposits found in human AD provided the murine APP gene harbors mutations linked to human FAD.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available