Expression of human FE65 in amyloid precursor protein transgenic mice is associated with a reduction in β-amyloid load
| Autor: | Charles Duyckaerts, Laurent Pradier, Nathalie Touchet, Luc Mercken, Nicolas Sergeant, André Delacourte, Gunter Tremp, Dominique Santiard-Baron, Dominique Langui, Benoît Delatour, Véronique Blanchard, Brigitte Schombert, Maryse Delehedde, Marie-Françoise Paul |
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| Rok vydání: | 2005 |
| Předmět: |
Genetically modified mouse
0303 health sciences medicine.medical_specialty Amyloid biology Transgene P3 peptide Signal transducing adaptor protein Biochemistry Cell biology 03 medical and health sciences Cellular and Molecular Neuroscience 0302 clinical medicine medicine.anatomical_structure Endocrinology Cerebral cortex In vivo Internal medicine mental disorders medicine Amyloid precursor protein biology.protein 030217 neurology & neurosurgery 030304 developmental biology |
| Zdroj: | Journal of Neurochemistry. 93:330-338 |
| ISSN: | 0022-3042 |
| DOI: | 10.1111/j.1471-4159.2005.03026.x |
| Popis: | FE65 is an adaptor protein that interacts with the cytoplasmic tail of the amyloid precursor protein (APP). In cultured non-neuronal cells, the formation of the FE65-APP complex is a key element for the modulation of APP processing, signalling and beta-amyloid (Abeta) production. The functions of FE65 in vivo, including its role in the metabolism of neuronal APP, remain to be investigated. In this study, transgenic mice expressing human FE65 were generated and crossbred with APP transgenic mice, known to develop Abeta deposits at 6 months of age. Compared with APP mice, APP/FE65 double transgenic mice exhibited a lower Abeta accumulation in the cerebral cortex as demonstrated by immunohistochemistry and immunoassay, and a lower level of APP-CTFs. The reduced accumulation of Abeta in APP/FE65 double transgenics, compared with APP mice, could be linked to the low Abeta42 level observed at 4 months of age and to the lower APP-CTFs levels. The present work provides evidence that FE65 plays a role in the regulation of APP processing in an in vivo model. |
| Databáze: | OpenAIRE |
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