Title |
Normal cognition in transgenic BRI2-Aβ mice
|
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Published in |
Molecular Neurodegeneration, May 2013
|
DOI | 10.1186/1750-1326-8-15 |
Pubmed ID | |
Authors |
Jungsu Kim, Paramita Chakrabarty, Amanda Hanna, Amelia March, Dennis W Dickson, David R Borchelt, Todd Golde, Christopher Janus |
Abstract |
Recent research in Alzheimer's disease (AD) field has been focused on the potential role of the amyloid-β protein that is derived from the transmembrane amyloid precursor protein (APP) in directly mediating cognitive impairment in AD. Transgenic mouse models overexpressing APP develop robust AD-like amyloid pathology in the brain and show various levels of cognitive decline. In the present study, we examined the cognition of the BRI2-Aβ transgenic mouse model in which secreted extracellular Aβ1-40, Aβ1-42 or both Aβ1-40/Aβ1-42 peptides are generated from the BRI-Aβ fusion proteins encoded by the transgenes. BRI2-Aβ mice produce high levels of Aβ peptides and BRI2-Aβ1-42 mice develop amyloid pathology that is similar to the pathology observed in mutant human APP transgenic models. |
X Demographics
Geographical breakdown
Country | Count | As % |
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United States | 1 | 50% |
United Kingdom | 1 | 50% |
Demographic breakdown
Type | Count | As % |
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Members of the public | 2 | 100% |
Mendeley readers
Geographical breakdown
Country | Count | As % |
---|---|---|
United States | 1 | <1% |
Unknown | 178 | 99% |
Demographic breakdown
Readers by professional status | Count | As % |
---|---|---|
Student > Ph. D. Student | 36 | 20% |
Student > Bachelor | 36 | 20% |
Student > Master | 18 | 10% |
Researcher | 17 | 9% |
Professor | 9 | 5% |
Other | 15 | 8% |
Unknown | 48 | 27% |
Readers by discipline | Count | As % |
---|---|---|
Neuroscience | 35 | 20% |
Biochemistry, Genetics and Molecular Biology | 26 | 15% |
Agricultural and Biological Sciences | 25 | 14% |
Medicine and Dentistry | 9 | 5% |
Psychology | 8 | 4% |
Other | 22 | 12% |
Unknown | 54 | 30% |