Genetic deletion of nitric oxide synthase 2 ameliorates Parkinson's disease pathology and neuroinflammation in a transgenic mouse model of synucleinopathy.

ABSTRACT: 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 α-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 α-synuclein phosphorylation at serine 129 and reduced α-synuclein-induced microglial and astrocyte activation in Syn^A53T/NOS^-/- mice. Additionally, neuroinflammation-related gen

SUBMITTER: Kim J 

PROVIDER: S-EPMC9841612 | biostudies-literature | 2023 Jan

REPOSITORIES: biostudies-literature