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. 2012 May 13;69(14):2409–2427. doi: 10.1007/s00018-012-1015-4

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, beta amyloid, LPS Lipopolysaccharide, MPTP 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine, ROS reactive oxygen species