| First Author | Ayton S | Year | 2015 |
| Journal | J Neurosci | Volume | 35 |
| Issue | 8 | Pages | 3591-7 |
| PubMed ID | 25716857 | Mgi Jnum | J:219846 |
| Mgi Id | MGI:5629865 | Doi | 10.1523/JNEUROSCI.3439-14.2015 |
| Citation | Ayton S, et al. (2015) Parkinson's disease iron deposition caused by nitric oxide-induced loss of beta-amyloid precursor protein. J Neurosci 35(8):3591-7 |
| abstractText | Elevation of both neuronal iron and nitric oxide (NO) in the substantia nigra are associated with Parkinson's disease (PD) pathogenesis. We reported previously that the Alzheimer-associated beta-amyloid precursor protein (APP) facilitates neuronal iron export. Here we report markedly decreased APP expression in dopaminergic neurons of human PD nigra and that APP(-/-) mice develop iron-dependent nigral cell loss. Conversely, APP-overexpressing mice are protected in the MPTP PD model. NO suppresses APP translation in mouse MPTP models, explaining how elevated NO causes iron-dependent neurodegeneration in PD. |
