| First Author | Kim J | Year | 2023 |
| Journal | Mol Brain | Volume | 16 |
| Issue | 1 | Pages | 7 |
| PubMed ID | 36647152 | Mgi Jnum | J:339845 |
| Mgi Id | MGI:7427959 | Doi | 10.1186/s13041-023-00996-1 |
| Citation | Kim J, et al. (2023) Genetic deletion of nitric oxide synthase 2 ameliorates Parkinson's disease pathology and neuroinflammation in a transgenic mouse model of synucleinopathy. Mol Brain 16(1):7 |
| abstractText | Studies of mouse models of Alzheimer's disease (AD) have demonstrated that nitric oxide synthase 2 (NOS2) is involved in AD pathology. However, the effects of NOS2 on the pathology of Parkinson's disease (PD) are not well studied. To address this gap, we examined the impact of NOS2 on disease-associated phenotypes in a mouse model of PD. Transgenic mice carrying the A53T mutation of alpha-synuclein (Syn(A53T)) and newly generated double transgenic mice with deletion of NOS2 (Syn(A53T)/NOS2(-/-)) were used. Compared with Syn(A53T) mice, the loss of nos2 decreased alpha-synuclein phosphorylation at serine 129 and reduced alpha-synuclein-induced microglial and astrocyte activation in Syn(A53T)/NOS(-/-) mice. Additionally, neuroinflammation-related gene clusters in the deep mesencephalic nucleus (DpMe) were altered in Syn(A53T)/NOS(-/-) mice compared with Syn(A53T) mice. Taken together, our results suggest that deletion of nos2 alleviates alpha-synuclein pathology and alpha-synuclein-associated neuroinflammatory responses in the brain. |
