Publication

Mutant and native human beta-amyloid precursor proteins in transgenic mouse brain

Howland, David S.
Savage, Mary J.
Huntress, Frederick A.
Wallace, Racheal E.
Schwartz, Daniel A.
Loh, Tamalette
Melloni, Richard H.
DeGennaro, Louis J.
Greenberg, Barry D.
Siman, Robert
Embargo Expiration Date
Abstract

Human beta-amyloid precursor protein (beta APP) has been targeted to transgenic neurons using synapsin I promoter-based chimeric transgenes. Native human beta APP was introduced as well as beta APP containing mutations genetically linked to familial Alzheimer's disease (AD) and to hereditary cerebral hemorrhage with amyloidosis-Dutch type. In mouse brain, human beta APP RNA was up to 60% as abundant as total endogenous beta APP RNA. Human beta APP gene expression was most abundant in the CA subfields of the hippocampus and in the piriform cortex. Correct processing of human beta APP at the beta-secretase cleavage site was demonstrated in transgenic mouse brains. Despite a 40% increase in total beta APP immunoreactivity in lines expressing mutant human beta APP, no evidence of amyloid deposition was found in brains of mice up to 14 months in age. Higher levels of mutant human beta APP, increased age, or other factors may be necessary to elicit beta-amyloid-related neuropathologies in the rodent brain.

Source

Neurobiol Aging. 1995 Jul-Aug;16(4):685-99.

Year of Medical School at Time of Visit
Sponsors
Dates of Travel
DOI
10.1016/0197-4580(95)00078-S
PubMed ID
8544921
Other Identifiers
Notes
Funding and Acknowledgements
Corresponding Author
Related Resources
Related Resources
Repository Citation
Rights
Distribution License