| First Author | Li B | Year | 2021 |
| Journal | Neurosci Lett | Volume | 764 |
| Pages | 136222 | PubMed ID | 34500002 |
| Mgi Jnum | J:312983 | Mgi Id | MGI:6792606 |
| Doi | 10.1016/j.neulet.2021.136222 | Citation | Li B, et al. (2021) Flavin-containing monooxygenase 1 deficiency promotes neuroinflammation in dopaminergic neurons in mice. Neurosci Lett 764:136222 |
| abstractText | A growing body of evidence indicates an association between flavin-containing monooxygenase (FMO) and neurodegeneration, including Parkinson's disease (PD); however, the details of this association are unclear. We previously showed that the level of Fmo1 mRNA is decreased in an in vitro rotenone model of parkinsonism. To further explore the potential involvement of FMO1 deficiency in parkinsonism, we generated Fmo1 knockout (KO) mice and examined the survival of dopaminergic neurons and relative changes. Fmo1 KO mice exhibited loss of tyrosine hydroxylase-positive neurons, decreased levels of tyrosine hydroxylase and Parkin proteins, and increased levels of pro-inflammatory cytokines (IL1beta and IL6) in the nigrostriatal region. Moreover, the protein levels of PTEN induced kinase 1 (PINK1) and p62, and the Microtubule associated protein 1 light chain 3 (LC3)-II/I ratio were not significantly altered in Fmo1 KO mice (P > 0.05). FMO1 deficiency promotes neuroinflammation in dopaminergic neurons in mice, thus may plays a potential pathological role in dopaminergic neuronal loss. These findings may provide new insight into the pathogenesis of PD. |
