Table 2.
Genetic deletion of NOX2 in murine models of Alzheimer’s and Parkinson’s disease is anti-inflammatory and neuroprotective
| Mouse disease model | Effect | References |
|---|---|---|
| Alzheimer’s disease | ||
| Aβ1-40 superfusion | Gp91−/− mice showed lower ROS and reduced cerebrovascular dysfunction | [181] |
| Tg2576/Cybb−/− mice | Lack of gp91 protected against neurovascular and behavioral dysfunction | [184] |
| Parkinson’s disease | ||
| Paraquat | Gp91−/− mice showed reduced microglial activation and DA neurotoxicity | [102, 129] |
| Neuromelanin | Gp91−/− mice showed reduced neuroinflammation and DA neurotoxicity | [99] |
| LPS | Gp91−/− mice showed reduced microglial activation and DA neurotoxicity | [26] |
| MPTP | Gp91−/− mice showed microglial activation and DA neurotoxicity | [143, 156] |
Genetic ablation of NOX2 in mice is associated with anti-inflammatory and neuroprotective effects in mouse models of Alzheimer’s and Parkinson’s disease
DA dopaminergic, Aβ beta amyloid, LPS Lipopolysaccharide, MPTP 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, ROS reactive oxygen species