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Table 2 Animal studies using genetic manipulations of NADPH oxidases on neurodegenerative disorders

From: NADPH oxidase in brain injury and neurodegenerative disorders

Disorder Animal model Genetic manipulation Manipulation Result References
Alzheimer’s Disease 1–42 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]