| First Author | Cannavo C | Year | 2022 |
| Journal | PLoS One | Volume | 17 |
| Issue | 5 | Pages | e0262558 |
| PubMed ID | 35544526 | Mgi Jnum | J:325631 |
| Mgi Id | MGI:7278205 | Doi | 10.1371/journal.pone.0262558 |
| Citation | Cannavo C, et al. (2022) Endosomal structure and APP biology are not altered in a preclinical mouse cellular model of Down syndrome. PLoS One 17(5):e0262558 |
| abstractText | Individuals who have Down syndrome (trisomy 21) are at greatly increased risk of developing Alzheimer's disease, characterised by the accumulation in the brain of amyloid-beta plaques. Amyloid-beta is a product of the processing of the amyloid precursor protein, encoded by the APP gene on chromosome 21. In Down syndrome the first site of amyloid-beta accumulation is within endosomes, and changes to endosome biology occur early in Alzheimer's disease. Here, we determine if primary mouse embryonic fibroblasts isolated from a mouse model of Down syndrome can be used to study endosome and APP cell biology. We report that in this cellular model, endosome number, size and APP processing are not altered, likely because APP is not dosage sensitive in the model, despite three copies of App. |
