From: NADPH oxidase in brain injury and neurodegenerative disorders
Disorder | Animal model | Genetic manipulation | Manipulation Result | References |
---|---|---|---|---|
Alzheimer’s Disease | Aβ1–42 injection | p47phox −/− | ↑M2 microglial phenotype (Ym1) ↓Monocyte chemoattractant (CCL2) | [205] |
Tg2576 | Nox2 −/− | ↓Cerebrovascular dysfunction & ROS ↑Cognition | [407] | |
Tg2576 Aβ1–40 injection | Nox2 −/− | ↓ROS & vascular dysfunction | [204] | |
APP-expressing neuroblastoma | Nox2 −/− macrophages (PLB-985 X-CGD) | Macrophages unable to kill APP-expressing neuroblastoma cells | [408] | |
Stroke | tMCAO | Nox1 −/− | ↑Cortical (but not total) infarct | [59] |
tMCAO | Nox1 −/− | ↓Lesion, edema & BBB disruption | [409] | |
pMCAO | Nox1 −/− | No change in infarct size | [409] | |
tMCAO | Nox1 −/− | No change in infarct size or outcome | [140] | |
tMCAO | Nox2 −/− | No change in infarct size or outcome | [140] | |
tMCAO | Nox4 −/− | ↓Infarct, edema & BBB disruption ↑Cognition/basal motor function | [140] | |
pMCAO | Nox4 −/− | ↓Infarct & functional deficits | [140] | |
tMCAO | Nox2 −/− | ↓Infarct | [160] | |
tMCAO | Nox2 −/− | ↓Lesion & BBB disruption | [158] | |
Perinatal Hypoxia-Ischemia (HI) | Nox2 −/− | No change in infarct size (severe hypoxia); ↑Infarct (moderate ischemia) | [410] | |
tMCAO | Nox2 −/− | ↓Infarct & spectrin cleavage ↑Neurological outcome | [131] | |
tMCAO | Nox2 −/− | ↓Infarct & inflammation | [157] | |
tBCCAO SAH | p47phox −/− Nox2 −/− | ↓CA1 neuronal degeneration No change in mortality, brain water content, or intensity of oxidative stress | [411] [172] | |
ICH | Nox2 −/− | ↓Hematoma, edema, deficits, mortality | [171] | |
Traumatic Brain Injury | CCI | Nox2 −/− | ↓Lesion, apoptosis & ROS | [185] |
SBI | Nox2 −/− | ↑Neurological outcome | [412] | |
Parkinson’s Disease | 6-OHDA | Nox2 −/− | ↑Neurological outcome & resistance to neurotoxicity | [227] |
MPTP | Nox2 −/− | Neuroprotective | [218] | |
MPP+ | Nox2 −/− neuron-glia culture | ↓Dopaminergic neurodegeneration | [221] | |
6-OHDA | Nox2 −/− | ↓Rotational behavior | [217] | |
Paraquat | NOX1 −/− differentiated human dopaminergic cells | ↓α-synuclein expression & aggregation | [226] | |
Paraquat | Nox1 shRNA | ↓α-synuclein expression & aggregation, ROS, dopaminergic neuronal loss | [226] | |
Amyotrophic Lateral Sclerosis | SOD1G93A | Nox2 −/− | ↓ROS, protein carbonylation, neurodegeneration ↑Longevity | [262] |
SOD1G93A | Nox1 −/− | Delayed disease progression ↑Survival | [276] | |
SOD1G93A | Nox2 −/− | Delayed disease progression ↓Muscle atrophy ↑Survival | [276] | |
SOD1G93A | Nox1 +/− or Nox2 +/− | ↑Survival | [276] | |
Huntington’s Disease | HD140Q/140Q | Nox2 −/− | ↑Neuronal viability ↓ROS | [246] |
Multiple Sclerosis | MOG induced EAE | p47phox −/− BV-2-myelin culture | ↓ROS, neuroinflammation | [308] |
MOG induced EAE | Nox2 −/− | ↓Weight loss, microglial reactivity ↑Oligodendrocyte survival, neurological outcome | [311] | |
 | MOG induced EAE | p47phox −/− | ↓EAE presentation | [309] |
MOG induced EAE | p47phox splice mutation | Enhanced EAE presentation | [310] |