TABLE 3

Cathepsin B Knockout Improves Behavioral Deficits in Animal Models of Neurologic Disorders

Neurologic Disease Mouse Model, Age, SexCathepsin B Knockout in the Neurologic Disease Model Improves OutcomesReferences
BehaviorsCell PathologyBiomarkers
Traumatic brain injury: controlled cortical impact mouse model, 15–28 weeks old, male↓Neuromotor deficits↓Brain tissue loss, ↓cell death in hippocampus↓Proapoptotic BaxHook et al., 2014a
Hypoxia-ischemia: neonatal HI mouse model, neonatal, sex not specifiednd↓Cell death in hippocampus, ↓neuroinflammation↓NF-κB to reduce inflammatory cytokinesNi et al., 2015
Epilepsy: EPM1, cystatin B KO mouse model, 2, 4, and 8 months old, sex not specifiedNo effect on seizures↓Cell death in neuronal granule cellsndHouseweart et al., 2003
Multiple sclerosis: EAE mouse model, 8–10 weeks old, female↑Clinical score, ↑ time of disease onset↓Infiltrating immunologic cells, ↓antigen presentationndAllan and Yates, 2015
Inflammatory pain: CFA model, 5 weeks old, male↓Allodynia behavioral test for pain↓Microglia cell size morphology, ↓decreased microglia extensionsBlockade of CFA-induced increase in IL-1β, IL-18, and COX-2Sun et al., 2012
Tolerance to opioid: chronic morphine antinociceptive tolerance, 10 weeks old, malePrevents opiate tolerance, ↓pain assessed by thermal hot plate test↓Elevation in excitatory postsynaptic potential↓Glutamate release from spinal neuronsHayashi et al., 2014
  • nd, not determined.