TABLE 3

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

Neurologic Disease Mouse Model, Age, Sex	Cathepsin B Knockout in the Neurologic Disease Model Improves Outcomes			References
Neurologic Disease Mouse Model, Age, Sex	Behaviors	Cell Pathology	Biomarkers	References
Traumatic brain injury: controlled cortical impact mouse model, 15–28 weeks old, male	↓Neuromotor deficits	↓Brain tissue loss, ↓cell death in hippocampus	↓Proapoptotic Bax	Hook et al., 2014a
Hypoxia-ischemia: neonatal HI mouse model, neonatal, sex not specified	nd	↓Cell death in hippocampus, ↓neuroinflammation	↓NF-κB to reduce inflammatory cytokines	Ni et al., 2015
Epilepsy: EPM1, cystatin B KO mouse model, 2, 4, and 8 months old, sex not specified	No effect on seizures	↓Cell death in neuronal granule cells	nd	Houseweart et al., 2003
Multiple sclerosis: EAE mouse model, 8–10 weeks old, female	↑Clinical score, ↑ time of disease onset	↓Infiltrating immunologic cells, ↓antigen presentation	nd	Allan and Yates, 2015
Inflammatory pain: CFA model, 5 weeks old, male	↓Allodynia behavioral test for pain	↓Microglia cell size morphology, ↓decreased microglia extensions	Blockade of CFA-induced increase in IL-1β, IL-18, and COX-2	Sun et al., 2012
Tolerance to opioid: chronic morphine antinociceptive tolerance, 10 weeks old, male	Prevents opiate tolerance, ↓pain assessed by thermal hot plate test	↓Elevation in excitatory postsynaptic potential	↓Glutamate release from spinal neurons	Hayashi et al., 2014