| First Author | Shen X | Year | 2019 |
| Journal | Biochem Biophys Res Commun | Volume | 512 |
| Issue | 4 | Pages | 653-658 |
| PubMed ID | 30791980 | Mgi Jnum | J:291733 |
| Mgi Id | MGI:6443148 | Doi | 10.1016/j.bbrc.2019.01.119 |
| Citation | Shen X, et al. (2019) Iron treatment inhibits Abeta42 deposition in vivo and reduces Abeta42/Abeta40 ratio. Biochem Biophys Res Commun 512(4):653-658 |
| abstractText | Alzheimer's disease (AD) is characterized by the formation of extracellular amyloid plaques containing the amyloid beta-protein (Abeta) within the parenchyma of the brain. Abeta42, which is 42 amino acids in length, is considered to be the key pathogenic factor in AD. Iron deposition is found abundantly in the amyloid plaques of AD patients; however, whether iron intake exacerbates amyloid deposition in vivo is unknown. Here, we treated AD model mice with iron-containing water and found that Abeta42 deposition in the brain was significantly inhibited, along with a decrease in iron deposition. Iron treatment did not change the overall levels of iron in the brain or serum. Interestingly, Abeta40 generation was significantly increased by iron treatment in amyloid precursor protein (APP)-overexpressing fibroblasts, whereas Abeta42 generation did not change, which led to a decreased Abeta42/Abeta40 ratio. Because Abeta40 can inhibit Abeta42 aggregation in vitro, and Abeta40 inhibits amyloid formation in vivo, our results suggest that iron can selectively enhances Abeta40 generation and inhibit amyloid deposition by reducing the Abeta42/Abeta40 ratio. Thus, iron may be used as a novel treatment for reducing the Abeta42/Abeta40 ratio and Abeta42 deposition in AD. |
